Dieting Nutrition Obesity

Adding Bitter Flavors to Decrease Glucose intake | Medical Weight Loss Alexandria Virginia

The above is a video from Wholistic matters. There was a recent study from the AHA demonstrating that individuals with differences in the ability to taste bitter may have altered intake of vegetables, which generally have a bitter taste.

Different variants of the taste gene TAS2R38 are the source of the bitter perception. There are two primary variants : an AVI and PAV Varianta. The AVI variant does not perceive bitter taste as much and was found that individuals with this SNP consumed more vegetables.

Individuals whose genetic code is written to perceive certain plant compounds as particularly bitter are less likely to eat vegetables. This is according to data analysis from 175 submissions to a food frequency questionnaire, where researchers associated certain eating habits with different variants of the taste gene TAS2R38. This research was presented as part of the American Heart Association Scientific Sessions 2019.

Is Taste Perception Genetic?

Humans have numerous receptors in the body that are responsible for taste perception, and the TAS2R38 gene encodes a protein that controls the perception of certain bitter tasting compounds of Brassica plants, also known as cruciferous vegetables. Specifically, the TAS2R38 bitter taste receptor manages the taste of certain glucosinolates, a type of phytonutrient found in cruciferous vegetables such as broccoli, cabbage, kale, and Brussels sprouts.

Many variants of the TAS2R38 gene have been identified worldwide, but two predominant common forms exist with vastly different effects on bitter perception: “PAV” and “AVI.” An individual with two copies of the AVI variant will be less likely to perceive bitter tastes from bitter compounds, while an individual with two copies of PAV will find bitter compounds extremely bitter. Someone with one copy of each variant will perceive bitterness somewhere in the middle of the spectrum.

In the recent study, researchers found that people with two copies of the PAV gene were 2.5 times more likely to “rank in the bottom half of participants on the number of vegetables eaten,” presumably because these individuals find bitter compounds in many vegetables unpalatable and unpleasant.

Are Bitter Foods Good for You?

As explained in this animation, “Managing Glucose Response With Bitter Nutrition,” bitter compounds are important for carbohydrate processing. The small intestine is lined with both glucose transporters and bitter receptors. Carbohydrates are metabolized into glucose, which is absorbed into the blood via glucose transporters, and compounds from bitter-tasting foods bind bitter receptors to help regulate glucose transport. When the diet contains excessive glucose and insufficient bitter compounds, chronically elevated blood glucose levels can lead to chronic conditions like obesity, metabolic syndrome, and diabetes.

What Foods are Bitter Tasting?

Plant-based foods with bitter compounds include cruciferous and green leafy vegetables (broccoli, Brussels sprouts, and kale), soybeans, citrus fruit (grapefruit, orange, lemon, and lime), green tea, red wine, and oats. Plant-based foods are often perceived as bitter because they contain phytonutrients, which have bitter properties. Plants produce phytonutrients as a protective mechanism, and when humans consume them, they reap health benefits as well. Plant-based phytonutrients are associated with the prevention of chronic conditions.

What Does Processing Do to Food?

Because many people perceive bitter compounds as disagreeable, food processing removes many naturally occurring bitter compounds. In this podcast, “Phytochemicals, Bitter Receptors, and Carbohydrate Processing,” Slavko Komarnytsky, PhD, describes how food technology of the last century engaged special food processing that removes bitter compounds from food to make it more enjoyable. Consuming processed food that has been “de-bittered” prevents bitter compounds from interacting with bitter receptors in the small intestine and regulating healthy carbohydrate processing.

Historically, in the absence of refined grains and unnaturally large pieces of fruit, human intake of carbohydrates was low. But with crop domestication and agricultural techniques of the past few decades, humans have exponentially greater access to carbohydrates, and the human body struggles to manage this influx of carbohydrates.

For more on bitter compounds and modern day breeding practices that affect natural sources of bitter compounds, listen to the podcast with Eric Jackson, PhD: Oats, Bitter Compounds, and a Lifetime of Plant Study.

How Can the Study of Genetics Improve Health?

Researchers from the American Heart Association presentation hope to expand upon their current study by using genetics to predict which vegetables people will like based on their TAS2R38 profile. And for people with two copies of PAV, genetic studies could help researchers identify certain spices to improve palatability of bitter foods. The better a food tastes, the more likely the average human will eat it. The more vegetables a person eats, the better.

AHA article on bitter tastes

Depression

New Treatments for depression in Alexandria, Virginia

CONTACT NOVA Health Ketamine Center: 703-844-0184 | Depression Treatment Center

Depression Medications

Medication can be an effective intervention for treating the symptoms of depression. Not all antidepressants, however, work the same way. The antidepressant your doctor will prescribe you often depends on your particular symptoms of depression, potential side effects, and other factors.

Most antidepressants work by affecting chemicals in the brain known as neurotransmitters. The neurotransmitters serotonin, norepinephrine, and dopamine are associated with depression. How medications affect these neurotransmitters determines the class of antidepressants to which they belong.

Types of Antidepressants (List of Medications)

Selective serotonin reuptake inhibitors (SSRIs) – SSRIs are the most commonly prescribed type of antidepressants. They affect serotonin in the brain, and they’re likely to have fewer side effects for most people. SSRIs can include citalopram (Celexa), escitalopram (Lexapro), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft).

Serotonin and norepinephrine reuptake inhibitors (SNRIs) – SNRIs are the second most commonly prescribed type of antidepressants. SNRIs can include duloxetine (Cymbalta), desvenlafaxine (Pristiq), levomilnacipran (Fetzima), and venlafaxine (Effexor).

Norepinephrine-dopamine reuptake inhibitors (NDRIs) – Bupropion (Wellbutrin) is the most commonly prescribed form of NDRI. It has fewer side effects than other antidepressants and is sometimes used to treat anxiety.

Tricyclic antidepressants – Tricyclics are known for causing more side effects than other types of antidepressants, so they are unlikely to be prescribed unless other medications are ineffective. Examples include amitriptyline (Elavil), desipramine (Norpramin), doxepin (Sinequan), imipramine (Tofranil), nortriptyline (Pamelor), and protriptyline (Vivactil).

Monoamine oxidase inhibitors (MAOIs) – MAOIs have more serious side effects, so they are rarely prescribed unless other medications do not work. MAOIs have many interaction effects with foods and other medications, so people who take them may have to change their diet and other medications. SSRIs and many other medications taken for mental illness cannot be taken with MAOIs.

Other antidepressants that don’t fit into a category are known as atypical antidepressants.

Medication

The medication prescribed is usually an antidepressant. A primary care practitioner can probably prescribe one. Factors the doctor will consider include other medical conditions, other medicines the patient is taking, side effects, and cost.

Practitioners typically start with a low dose that is gradually increased until improvement is shown. First-time antidepressants may take 4 to 6 weeks to show improvement. The doctor will monitor the side effects and measure improvement.Article continues below

Do you feel depressed?

Take one of our 2-minute Depression quizzes to see if you or a loved one could benefit from further diagnosis and treatment.Take Depression QuizTake Partner Depression Quiz

Types of Medication and Treatments

  • Selective Serotonin Reuptake Inhibitors (SSRIs) SSRIs relieve symptoms by blocking the absorption (called “reuptake”) of serotonin by particular brain nerve cells. Because serotonin helps regulate mood, an SSRI helps leave more serotonin available. Most common drugs prescribed for depression, including fluoxetine (Prozac®), paroxetine (Paxil®, Pexeva®), sertraline (Zoloft®), citalopram (Celexa®), and escitalopram (Lexapro®). Side effects: insomnia (sleeplessness), sexual dysfunction, and weight gain, but fewer side effects than tricyclic antidepressants (see below).
  • Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs) work with a double type of action by increasing levels of serotonin and norepinephrine that inhibit these chemicals being absorbed back into brain cells. Examples: duloxetine (Cymbalta®), venlafaxine (Effexor XR®), desvenlafaxine (Pristiq®, Khedezla®), levomilnacipran (Fetzima®). Side effects: headache, nausea or upset stomach, a minor increase in blood pressure, weight gain, sexual dysfunction.
  • Norepinephrine-Dopamine Reuptake Inhibitors (NDRIs) help increase the concentrations of mood regulators in the brain. Examples: bupropion (Wellbutrin®, Aplenzin®, Forfivo XL®) and Mirtazapine (Remeron®). NDRIs may produce fewer side effects, or side effects may be different. Bupropion can cause anxiety but causes the least sexual side effects. Mirtazapine may also produce fewer sexual side effects and less nausea, but it causes weight gain and sedation.
  • Tricyclic Antidepressants (TCAs) include imipramine (Tofranil®), nortriptyline (Pamelor), amitriptyline, doxepin, and desipramine (Norpramin®). Tricyclics tend to cause more side effects than newer antidepressants.TCAs work similarly to SNRIs, but they produce even more side effects. Conversely, they may ease chronic pain. Tricyclics may be prescribed when patients have tried other medications that have not worked.
  • Monoamine Oxidase Inhibitors (MAOIs) include drugs such as tranylcypromine (Parnate®), phenelzine (Nardil®) and isocarboxazid (Marplan®). May be prescribed when other medications haven’t worked but can have serious side effects. MAOIs usually require a strict diet because of dangerous (or even deadly) interactions with foods (cheese, pickles, wine). MAOIs may also produce a bad reaction when taken with medications such as decongestants, birth control pills, and some herbal supplements. MAOIs can never be combined with SSRIs.
  • Atypical Antidepressants. These medications do not belong to any of the common categories of antidepressants. These include trazodone, vortioxetine (Trintellix®), and vilazodone (Viibryd®). Sometimes they have novel mechanisms of action that are under development, and sometimes they act more rapidly than typical antidepressants.
  • Atypical Antipsychotics (Second-Generation Antipsychotics, or SGAs). These drugs are also called second-generation antipsychotics (SGAs) and may be used for treatment-resistant depression (TRD) or very severe depressive disorder. These include aripiprazole (Abilify®), quetiapine (Seroquel® and Seroquel XR®), and olanzapine (Zyprexa®) — often used in combination with other medications including fluoxetine. Brexpiprazole (Rexulti®): is used to treat certain mental/mood disorders such as schizophrenia and depression and may also help to improve mood, sleep, appetite, and energy level.
  • Newly-Approved Antidepressants Selegiline (Emsam®), an MAOI that is put on your skin as a patch, may cause fewer side effects than other MAOIs. Another newly-approved antidepressant on the market is a ketamine nasal spray called Spravato.

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Other Medicinal Options

  • Lithium has long been used as a mood stabilizer; it is indicated for the treatment of bipolar disorder. Lithium reduces the risk of suicide in patients with bipolar or depression by more than 60%. Lithium is used to treat and prevent episodes of mania in people with bipolar disorder, also called manic-depressive disorder. It is called an “antimanic agent.”
  • Thyroid treatments: Thyroid hormone can be used in two different ways to treat unipolar major depression. Most often, thyroid hormone is used as augmentation for patients who respond insufficiently to antidepressant monotherapy and can also be started simultaneously with a tricyclic at the beginning of pharmacotherapy to accelerate response compared with tricyclic antidepressant monotherapy.
  • MDMA (aka “molly” or “ecstasy”) a psychoactive substance originally used for people with PTSD
  • Medical cannabis (marijuana): although clinical research in humans is not available, THC and CBD have been shown in animal models to be beneficial.
  • Psychedelics such as LSD and psilocybin (the psychoactive ingredient in mushrooms) are under study. Participants are closely monitored.

Brain Stimulation Therapies

  • Electroconvulsive Therapy (ECT): For treatment-resistant depression and severe depression, ECT involves transmitting short electrical impulses into the brain.
  • Repetitive Transcranial Magnetic Stimulation (rTMS) is brain stimulation similar to ECT, but it uses a magnet instead of electrical current.
  • Vagus Nerve Stimulation (VNS) is a treatment for major depressive disorder and treatment-resistant depression.
  • Deep Brain Stimulation (DBS), first approved for Parkinson’s, provides pulses of electricity from an implanted battery pack. It is approved to treat OCD but its use in depression remains experimental.

Treating Depression with Therapy

There are 3 common types of therapy available that have good track records for treating depression:

  • Cognitive Behavioral Therapy (CBT) helps assess and change negative thinking patterns associated with depression. The patient can learn coping strategies by recognizing negative thoughts. This is a structured therapy that is often limited to a certain number of visits, possibly 8-16 sessions.
  • Psychodynamic Therapy encourages the patient to look at negative behaviors and try to recognize and then change them. Its theory is that bad patterns and feelings are rooted in past experiences, which the therapist works with the patient and tries to tap the unconscious processes that have led to problems and then to help change them.
  • Interpersonal Therapy (IPT) looks at personal relationships and encourages the patient to make changes in life. The focus is to learn from the therapist how to improve problems and how to evaluate interactions to improve how they relate to others.

Treating Depression with Changes in Lifestyle

Changes in lifestyle and ridding yourself of old, unhealthy habits may be the most challenging part of treating your own depression. Here are some ways to improve your outlook:

  • Find a meaningful purpose in your life. Having a strong sense of purpose offers a buffer against inevitable setbacks and obstacles. Activities that connect you with something greater—pursuing a college degree or mastering a challenging task —can not only provide a goal to work toward but a healthy and meaningful distraction.
  • Cultivate social support. Personal connections with others (friends, family members, neighbors, etc.) provide many people with a reason to get up in the morning. Strong relationships help reduce isolation and loneliness. Join a class, make phone calls to people you’ve lost touch with, volunteer in a food kitchen or animal shelter, adopt a pet, and maintain contact with family and friends.
  • Develop coping skills to help reduce stress. Identifying what causes stress and avoiding those situations can help. Learning relaxation techniques in unavoidably-difficult settings (for example, family gatherings) will make a person less subject to depression
  • Get a sufficient amount of restorative sleep. The importance of quality, restorative sleep cannot be overstated. It helps maintain the brain’s function. Without adequate sleep, people are more likely to have negative thoughts and anxiety, leading to depression.
  • Make sure you move, every day. Regular engagement in physical activity—even a small amount—can make a big impact. Exercise not only boosts self-confidence but improves social connections, and increases self-esteem.
  • Eat clean. A diet that includes plenty of fresh whole foods, staying hydrated by consuming water throughout the day, cutting out sugary beverages and heavily-processed food, reducing caffeine and alcohol consumption can go a long way toward improving your mood.
  • Stay motivated to make difficult lifestyle changes by rewarding yourself occasionally with things you enjoy. Negative attitudes deplete chemicals in the brain that create contentment. Negativity also damages the immune system and upsets the body’s hormonal balance.
Depression Scopolamine Uncategorized

703-844-0184 | Ketamine Infusions D.C. Maryland Virginia | Scopolamine I.V. for rapid depression relief | Northern Virgina Ketamien Infusion Center Fairfax, Va

Scopolamine has been used in multiple forms (patches, tablets, nasal sprays, and IV)  for nausea, sea-sickness, and even depression.  It is a muscarinic acetylcholine receptor antagonist agent.

In 2006, Maura Fury, Ph.D. of the National Institutes of Mental Health treated anxiety and depression with I.V. Scopolamine with rapid results.

In the trial they evaluated the role of the cholinergic
system in cognitive symptoms of depression and unexpectedly
observed rapid reductions in depression severity
following the administration of the antimuscarinic drug
scopolamine hydrobromide (4 μg/kg intravenously) compared
with placebo (P=.002) In this trial, 9 patients with treatment resistant depression and anxiety received infusions and had significant repsonses,

The cholinergic system is one of the neurotransmitter systems implicated in the pathophysiologic mechanism of mood disorders. Increasing cholinergic activity using physostigmine (an anticholinesterase inhibitor) provides a challenge uniquely capable of exacerbating depressive symptom in currently depressed patients with MDD and inducing depressive symptoms
in currently manic patients with Bipolar disorder.

The cholinergic system also is implicated in depression by evidence showing that polysomnographic responses to muscarinic receptor agonists and neuroendocrine and pupillary responses to cholinomimetics are exaggerated in depressed patients and that some muscarinic receptor gene polymorphisms are associated with an elevated incidence of depression. Elevated cholinergic function thus was hypothesized to participate in
the pathogenesis of mood disorders.

In fact it has been noted that children growing up near sites of cholinergic pesticides have an increase rate of depression as the article above discusses.

A follow up study using Scopolamine was accomplished with 23 patinets and demonstrated rapid antidepressant and anti-anxiety effects with IV Scopolamine:

In the study, 23 subjects were treated. Here are the results:

Results—Following the initial block the group receiving scopolamine first (S/P) showed a 32 percent reduction in MADRS scores (p<0.001) which exceeded the corresponding change of 6.5 percent under placebo (P/S) (p=0.009), confirming the a priori hypothesis. Improvement was
significant at the first evaluation that followed scopolamine administration (p=0.011). In block 2 the P/S group showed a 53 percent reduction in MADRS scores (p=0.001) following scopolamine versus placebo, while the reduction seen in S/P subjects who received scopolamine during block 1
persisted as they received placebo during block 2. Scopolamine induced drowsiness, blurred vision, dry mouth, light-headedness and reduced blood pressure, which were sufficiently well tolerated that no subject dropped out due to side effects.

The trial included Bipolar disorder and depressed patients and used a protocol of 4 mcg/kg over 15 minutes protocol. No patients dropped out.Patient improved within 3-5 days of the infusion. The improvement in the study lasted well over two weeks.

Moreover, the delay in the onset of the antidepressant response until well after the resolution of anticholinergic side effects appears compatible with an effect on transcription of “late response” genes or synaptic plasticity, rather than a direct action on muscarinic receptors.

One effect scopolamine shares with other somatic antidepressant treatments involves the modulation of N-methyl-D-aspartate receptor (NMDAR) function. Blocking muscarinic receptors via scopolamine administration reduces mRNA concentrations for NMDAR types
1A and 2A in the rat brain in vivo and protects hippocampal neurons from glutamatemediated neurotoxicity in vitro . Chronic administration of antidepressant drugs from various classes and repeated electroconvulsive shock reduce cortical NMDAR function ), and treatments associated with a rapid onset of antidepressant effects either exert direct
NMDAR antagonist effects (ketamine) or induce NMDR internalization (sleepdeprivation)). Taken together with evidence that abnormal glutamatergic transmission is involved in the pathophysiology of depression, these data suggest the hypothesis that scopolamine’s effect on NMDAR function plays a role in its antidepressant action.

Another possible mechanism that merits consideration is scopolamine’s paradoxical effect of enhancing parasympathetic autonomic outflow when administered in the low dose range that encompasses the doses used in this study.

While it remains unclear whether the effect of scopolamine (at 4.0
ug/kg iv) on parasympathetic activity plays any role in the antidepressant response, it is noteworthy that the pathophysiology of depression is associated with a reduction in the parasympathetic-to-sympathetic balance. Decreasing parasympathetic tone improves depression.

Side effects during the infusion:

  • Blurry vision
  • Dry Mouth
  • Lowered Blood pressure
  • Nausea
  • Some confusion for two hours may occur but no delirium

Small but statistically significant antidepressant effects were observed the day following the administration of scopolamine 0.4 mg i.m., which would have a bioavailability similar to that of about 2 ug/kg i.v.

In 2012, researchers in Iran led by Danial Khajavi, M.D.,
compared 40 patients with MDD randomly assigned to either
oral scopolamine plus citalopram or citalopram plus placebo.
Augmentation with scopolamine was significantly more
effective than placebo, with 65 percent of patients receiving
scopolamine showing higher rates of response at week 4 and
remission at week 6 than patients receiving placebo.

Oral Scopolamine Augmentation in Moderate to Severe Major Depressive Disorder: A Randomized, Double-Blind, Placebo-Controlled Study:

Danial Khajavi, MD; Mehdi Farokhnia, MD; Amirhossein Modabbernia, MD; Mandana Ashrafi, MD; Seyed-Hesammedin Abbasi, MD; Mina Tabrizi, MD; and Shahin Akhondzadeh, PhD

Objective:To evaluate the antidepressant effect of oral scopolamine as an adjunct to citalopram.

Method:In this randomized double-blind placebo-controlled study, patients were assessed in the outpatient clinics of 2 large hospitals from November 2011 to January 2012. Forty patients (18–55 years) with major depressive disorder (DSM-IV-TR criteria) and 17-Item Hamilton Depression Rating Scale (HDRS) score ≥22 were randomly assigned to scopolamine hydrobromide (1 mg/d) (n=20) or placebo (n=20) in addition to citalopram for 6 weeks. HDRS score was measured at baseline and days 4, 7, 14, 28, and 42. The primary outcome measure was HDRS score change from baseline to week 6 in the scopolamine group versus the placebo group. Response was defined as ≥50% decrease in HDRS score; remission, as HDRS score ≤7.

Results: Augmentation with scopolamine was significantly more effective than placebo (F1,38=5.831, P=.021). Patients receiving scopolamine showed higher rates of response (65%, 13/20 at week 4) and remission (65%, 13/20 at week 6) than the placebo group (30%, 6/20 and 20%, 4/20, respectively; P=.027, P=.004, respectively). Patients in the scopolamine group showed higher rates of dry mouth, blurred vision, and dizziness than the placebo group.

Conclusions: Oral scopolamine is a safe and effective adjunct for treatment of patients with moderate to severe major depressive disorder.

General information regarding Treatment resistant Depression :

Carlos Zarate also did a review on Scopolamine for depression therapy:

They review the data from a series of randomized, double-blind, placebo-controlled studies involving subjects with unipolar or bipolar
depression treated with parenteral doses of scopolamine. The onset and duration of the antidepressant response are considered in light of scopolamine’s pharmacokinetic properties and an emerging literature that characterizes scopolamine’s effects on neurobiological systems beyond
the cholinergic system that appear relevant to the neurobiology of mood disorders. Scopolamine infused at 4.0 μg/kg intravenously produced robust antidepressant effects versus placebo, which were evident within 3 days after the initial infusion. Placebo-adjusted remission rates were 56%
and 45% for the initial and subsequent replication studies, respectively. While effective in male and female subjects, the change in depression ratings was greater in female subjects. Clinical
improvement persisted more than 2 weeks following the final infusion. The timing and persistence of the antidepressant response to scopolamine suggest a mechanism beyond that of direct muscarinic cholinergic antagonism. These temporal relationships suggest that scopolamineinduced
changes in gene expression and synaptic plasticity may confer the therapeutic mechanism.

Interest in the muscarinic cholinergic system in mood disorders stemmed initially from evidence suggesting that hyper-sensitivity of the cholinergic system plays a role in the pathophysiology of depression. Researchers showed that increasing cholinergic activity using the anticholinesterase inhibitor, physostigmine, provided a challenge uniquely capable
both of exacerbating depressive symptoms in currently depressed subjects with major depressive disorder (MDD) and inducing depressive symptoms and reversing manic symptoms in manic subjects with bipolar disorder (BD) . The neuroendocrine and pupillary responses to physostigmine) also were abnormally increased in depressed individuals. The muscarinic cholinergic receptor system specifically was implicated by
evidence showing that polysomnographic responses to selective muscarinic agonists were exaggerated in depressed versus control samples, suggesting that muscarinic receptor supersensitivity exists in depressed individuals

The muscarinic receptor system, variation in the type 2 muscarinic (M2) cholinergic receptor gene (CHRM2) was associated with an elevated incidence or severity of unipolar depression and with abnormal
reductions in M2 receptor binding in bipolar depression.

Some abnormalities in cholinergic receptor function in mood disorders showed sex effects. For example, sex differences manifested in the baseline and cholinergically stimulated plasma hormone measures that differed between depressed and control samples, suggesting that heightened cholinergic sensitivity exists preferentially in premenopausal females with
MDD . Comings et al. found that genetic variation in CHRM2 gene (A/T
1890) was associated with MDD specifically in female subjects. In rodents, estrogen enhanced choline acetyltransferase activity and acetylcholine release , and M2 receptor stimulation mediated the estrogen-induced enhancement of N-methyl-D-aspartate receptor (NMDAR) function (24). These observations complement evidence reviewed
below that women are more likely than men to show an antidepressant response to scopolamine.

Putative animal models of depression also supported a role for elevated muscarinic cholinergic function. Flinders Sensitive Line rats, bred selectively for increased sensitivity of muscarinic receptors, showed putative behavioral analogs of depression such as lethargy,
reductions in self-stimulation, and increased behavioral despair in the forced swim test in response to agents that increase central cholinergic function . Moreover, antimuscarinic agents (including scopolamine) produced antidepressant-like effects by reducing the
behavioral despair induced via this test.

The timing of the antidepresant effects was after the third day of the infusion.


Scopolamine conceivably may alter synaptic plasticity or gene expression through a variety of direct or indirect mechanisms. In addition to producing antagonist effects at muscarinic receptors, scopolamine acutely increases acetylcholine release (via inhibi tion of releasecontrolling
muscarinic autoreceptors) and thereby increases cholinergic effects on nicotinic receptor systems to an extent that conceivably may contribute to antidepressant or antiinflammatory
effects. In addition, changes in muscarinic tone specifically have been
shown to affect other depression relevant systems, including the central dopamine serotonin, and neuropeptide Y transmitter systems and the innate immune system. Thus,
the antidepressant mechanism(s) of scopolamine potentially may involve a variety of systems.
One effect of scopolamine that is shared by some other somatic antidepressant treatments involves modulation of NMDAR function. The NMDAR gene expression is enhanced by muscarinic receptor stimulation in at least some brain structures , and thus, the elevated
muscarinic receptor sensitivity identified in mood disorders may contribute to an elevation in NMDAR transmission. Blocking muscarinic receptors via scopolamine administration reduces messenger RNA concentrations for NMDAR types 1A and 2A in the rat brain in vivo and protects hippocampal neurons from glutamate-mediated neurotoxicity
in vitro . Chronic administration of TCAs and repeated electroconvulsive shock reduce cortical NMDAR function, and treatments associated with a rapid onset of antidepressant effects exert direct NMDAR antagonist effects (ketamine) or induce NMDAR internalization (sleep deprivation) . Given evidence that abnormal glutamatergic transmission is involved in the pathophysiology of depression, these datasuggest that scopolamine’s effect on reducing NMDAR gene expression may play a role in
its antidepressant action.

In the above article, women have a more robust response to scopolamine than men do.

When comparing the baseline block to study end, the blockgender interaction (F¼12.6, p¼0.001) showed that the antianxiety response was greater in women. Men and women show a rapid antidepressant response following scopolamine, but the magnitude of response is larger in women than in men.

The bottom line: Scopolamine offers another route of treatment for depression and anxiety. We offer IV Scopolamine infusions at NOVA Health as well as scopolamine /Beta Blocker oral treatment dor dperession add on therapy and anxiety.

Obesity Weight Loss

703-844-0184 | Medical Weight Loss Fairfax, Virginia| 7 things that prevent weight loss – notes | Ketamine NAD+ Vitamin Infusion Center Virginia

  • It is not about calories in and calories out – as some can exercise and eat less yet gain weight

Roadblocks to weight loss:

  • Liver toxicity

The liver detoxifies toxins and wastes and stores glycogen, amino acids and fats. It detoxifies by Phase 1 and Phase 2 detoxification. Each requires different compounds. Phase 1 needs folate, B2, B6, flavonoids, Glutathione, B12  and phase 2 needs Glyine, Taurine, B12, methionine, Cysteine, folic acid, Glutamine, Choline. Birth control pills deplete B6, Vegans are low in B12.

Signs of a Liver abnormality: sleep disturbance, foggy thinking, stiffness, blood sugar abnormalities, skin abnormalities, cholesterol issues, low energy.

Lemon in water | Increase fiber: flax seeds, psyllium, apple pectin, rice bean, oat fiberm chia seeds, sun fiber. Eat beets, apples, lemons, onion, cabbage, broccoli, Brussel sprouts, artichoke, milk thistle Herbs : dandelion root, artichoke, milk thistle, Turmeric.  Use ALA, Calcium D Glucarate, NAC, Selenium, Choline, Methionine.

  • Thyroid disorders

Low Thyroid: Hashimototo’s autoimmune, adrenal imbalance, estrogen dominance/progesterone deficiency, liver toxicity, food allergy, iron deficiency anemia, nutritional deficiencies( Zn/selenium, food allergy, Vitamin D deficiency, Candida overgrowth, heavy metal toxicity – lead cadmium, mercury stop T4-àT3 conversion. Low Metabolic rate with low thyroid.

TESTS: TSH, free T4, Free T3, TPO TSH

Identify heavy metal toxicity, and food allergy | zic and selenium for T4àT3 conversion | minerals such as Tyrosine, Iodine, Copper, Se, Zinc, Vitamin A and D3 \ Herbs Kelp, Ashwaganda, Blue Iris, Nettles, Coleus, Guggul | Use dessicated thyroid with T4/T3 in it

  • Estrogen dominance

Estrogen dominance due to infrequent ovulation, xeno estrogens, cysts of ovary, stress, obesity,, liver toxicity, B6/Magnesium deficient, Caffeine, HRT/BCP cause estrogen build up.

Estrogen reduces sensitivity of Thyroid receptors.

Symptoms: PMS, depression, anxiety, hot flashes, disturbed sleep, night sweats, weight gain, dry skin, fibromyalgia, fluid retention

Get estrogen: Progesterone ratio | reduce exposure to xeno estrogen (dry cleaners, household products, cleaners) | consume crucifers – broccoli, cauliflowers, cabbage, brussel sprouts, choy, arugula, mustard greens, water cress | Increase fiber – chia, psyillium., apple pectin, beet fiber, sun fiber, rice bran |

Detox for estrogen : Diindolemethane (DIM), Indole 3 Carbinnol, NAC, Calcium D Glucarate, Curcumin, Green Tea extract

Progesterone promotion with wild yam, Bupleurum , Passion Flower, Coleus Forkskohli, Peony root

  • Food allergies

Delayed onset food allergy IgG and IgA reactions 30 minutes and up to 3 days after exposure-

Elimination diet – glutein soy eggs shellfish citrus nightshade sugar alcohol caffeine, peanuts

Eliminate glutein for three months- take L Glutamine to promote gut healing and omega 3 to replaces deficiencies.

  • Hidden yeast issues

Yeast is kept in balance by good bacteria | Sugar craving | Digestive issues, vaginal infection, PMS, fibroid disorders, brain fogs, allergy, chemical insensitivities

Treatment: Candida Questionnaire | Probiotics | Vitamin D3, Zin, Selenium, Vitamin A, Omega 3 || Liver Detox – Calcium Glucarate, NAC, Burdock Root, Dandelion root, Artichoke  | Fiber – flax, psyllium, chia, apple pectin, sun fiber

  • Sleep and stress

Those who Sleep 5 hours or less per night gain weight – also get impulse control and decision making problems. Also you increase Ghrelin and decreases Leptin… Melatonin deficiency, cortisol excess, RLS (iron, B6, D3, C, E) Magnesium deficiency, thyroid, progesterone, estrogen, stress, caffeine, are sissues

GABA 200-500 mg, Relora 300 mg, 5HTP 300 mg before bedtime Take Phosphatidylserine. Valerian, passion flow, Hops, Lemon balm

Adrenal glands excrete cortisol in stress and causes fat and calorie storage, conservation of energy . Abdominal fat cells have more cortisol receptors than any part of the body.

Feeling tired and wired, difficulty sleeping, abdominal weight gain, muscle mass loss, anxiety – High cortisol

Low cortisol: Fatigue in the morning , infections, decreased exercise recovery, low blood sugar, burned out depression, low sex drive

For stress: balance blood sugar with meals every 3 hours, eliminate gluten, sugr, alcohol, caffeine, and dairy | Identify your stress. Get adequate sleep and gentle exercise, walking strectching, and swimming.

Take adrenal supporting herbs like : Licorice root, Ashwaghanda, Reolora, Rhodiola, Siberian Ginsengm Schisandra.

Take supplements to support the adrenal gland: Vitamin B complex, Vitamin C, Magnesium, Phosphatidyl Serine, and DHEA. Take adrenal cell extract

  • Insulin resistance

Insulin maintains balanced sugar and is secreted depending on what we eat.

What causes Insulin Resistance? Generally apple shaped body habitus – excess fat leads to insulin resistance .Results in elevated blood triglycerides, high blood pressure, high cholesterol.

At menopause, women seem to get a new body: changes in progesterone, estrogen, and testosterone as well as insulin levels change with insulin resistance. You need to balance DHEA, cortisol, thyroid, progesterone, estrogen and testosterone levels.

How to treat: 

Avoid juice, sweets, alcohol.  Avoid processed flour and deep fried foods.

Consume sugar balancing foods such as lean protein, omega 3, eggs, vegetables above ground, raw nuts, seeds, low glycemic foods, coconut oil, low glycemic legumes, garlic, and onions

Use herbs like turmeric, cinnamon, ginger, rosemary, basil, and oregano

Balance blood sugar with chromium, alpha lipoic acid, omega 3, biotin, and antioxidants

Consume extra fiber to reduce blood sugar and decrease appetite: Ground flax seeds, apple pectin, sun fiber, chia seeds, PGX fiber, oat fiber, and psyllium.

Exercise regularly 30 minutes per day

Omega 3 fatty acids are neded

Tests:

Hormone panel : Estradiol, Progesterone, testosterone, cortisolx4, DHEA, TSH, T4 free, t3 free and TPO

Sleep panel : cortisolx4 and melatonin x 4

Metabolic blood tests : CRP, fasting insulin, HbA1c, triglycerides, cholesterol total, VLDL, HDL

Food allergy blood tests : ELISA/EIA 94 IgG Panel

Candida – Blood, stool, urine and Candida Questionaire

What is Relora:

Relora
Promotes healthy cortisol and DHEA production, moderates occasional stress and promotes satiety when combined with a healthy diet and exercise

*Relora is a natural, proprietary blend of Magnolia officinalis and Phellodendron amurense. This synergistic combination of extracts helps promote positive mood and moderates occasional stress, in addition to supporting satiety and healthful eating. The magnolia and phellodendron fractions may bind to key central nervous system receptors, including those for GABA and the serotonin transporter, which encourages feelings of satiety and relaxation. A pilot clinical trial reported that Relora was well tolerated and helped promote emotional well being, muscle relaxation and moderated occasional stress. A follow-up trial reported similar results, as well as indicated that supplementing with Relora may help diminish stress-related sugary snack cravings and promote healthful eating habits. An animal study further demonstrated the supplements ability to support mood and relaxation. A recent pilot clinical trial performed in Cincinnati, Ohio, suggested that magnolia and phellodendron helped to maintain healthy cortisol and DHEA production and metabolism, which helped support healthy body-fat distribution.

Relora is a standardized blend of extracts from Phellodendron amurense and Magnolia officinalis that studies have indicated helps mediate everyday stress-related emotions, eating behavior, and muscle tension, without causing sedation. Supports central nervous system relaxation.

Vitamin Link:  https://www.nhc.com/

Hormones and explanations in weight Gain:

Estradiol (E2) at optimal physiological levels in women promotes a healthy distribution of fat in hips, thighs, breasts, and subcutaneously. However, in excess, and in the absence of progesterone, estrogen predisposes to unhealthy surplus weight gain in these tissues. Men generally have much lower levels of estradiol and higher testosterone, which is responsible for greater muscle mass and less fat distribution in areas of the body normally seen in women. In overweight men testosterone levels drop and estrogens rise leading to the same problematic weight gain in the hips, thighs, and breasts (referred to as gynecomastia) as seen in women .

Progesterone (Pg) in addition to its primary role in attenuating the effects of excess estrogen in the body by downregulating estrogen receptors, aids weight management by acting as a natural diuretic. Its natural calming effects in the brain may also reduce stress-related overeating and food cravings. As a mineralocorticoid receptor antagonist, progesterone counteracts the effects of mineralocorticoid activation, which include the stimulation of fat cell formation, increased body weight, and release of inflammatory cytokines. However, excessive supplementation with progesterone to higher than normal levels can increase appetite and also slow the rate of food emptying from the stomach and moving through the digestive tract, causing slower digestion and bloating.

Testosterone (T) and DHEA-S (DS) are androgens that increase lean muscle mass and metabolic rate. As androgen levels decline, muscle mass also decreases with a corresponding increase in adiposity. Low androgens can also reduce vitality and tolerance for exercise. Weight gain itself, with its resulting hormone imbalances, can trigger a drop in testosterone as the aromatase enzyme within fat tissue converts androgens to estrogens. In men this contributes to a femaletype body fat distribution, including breast tissue development. In women with polycystic ovarian syndrome (PCOS), high testosterone and DHEA are linked to insulin resistance and weight gain, particularly in the abdomen.

Cortisol (C) imbalances can create problems with blood sugar control, sleep patterns, appetite, food cravings, and tolerance exercise. Under stress, excessive cortisol production particularly in concert with insulin, promotes fat storage in abdominal adipose tissue. This visceral type of fat is closely associated with insulin resistance and metabolic syndrome and thus more hazardous to health. Chronically elevated cortisol is a known risk factor for pre-diabetes and cardiovascular disease.

Thyroid Stimulating Hormone (TSH) elevations, even within the high-normal range, are linked with hypothyroidism, low metabolic rate and obesity. Hypothyroidism is linked to elevated cortisol and can also be a consequence of oral estrogen therapy, which increases the production of binding proteins that reduce thyroid hormone bioavailability. Vitamin D (D2, D3) deficiency is common in obesity and particularly associated with hyperinsulinemia and visceral fat. Whether by cause or effect, identifying and correcting vitamin D3 deficiency may improve insulin sensitivity.

Fasting Insulin (In), when elevated, is a marker of insulin resistance which precedes metabolic syndrome, PCOS, and type 2 diabetes. Increased levels, particularly in concert with cortisol lead to central obesity and increased inflammatory and other cardiovascular disease markers. Hyperinsulinemia also contributes to decreased testosterone levels in men, but increased testosterone and decreased ovulation in women.

Hemoglobin A1c (HbA1c) is an indirect measure of the average circulating glucose levels over the previous three months. An HbA1c of more than 6% is predictive of type 2 diabetes and cardiovascular disease risk.

Hormone Weight Gain Connection

 Estrogen/progesterone imbalance: weight gain in hips, thighs; water retention; low thyroid/metabolism

 Testosterone/DHEA imbalance: decreased lean muscle, low metabolic rate; abdominal obesity

 Cortisol imbalance: increased appetite, sugar cravings, and belly fat; inhibits thyroid and metabolism

 Vitamin D3 deficiency: hyperinsulinemia; visceral fat

 TSH elevated: hypothyroidism, low metabolic rate, obesity

 Fasting Insulin: insulin resistance, abdominal obesity

 HbA1c: predictive of type 2 diabetes

Hormones And Weight Gain – Your Questions Answered

Candace BurchTuesday, February 17, 2015

Hormones And Weight Gain - Your Questions Answered

During the Balance Your Hormones to Balance Your Weight Webinar, many questions were asked that we couldn’t get to during the one hour presentation. We followed up with Candace Burch, and she took a few minutes to respond to your questions below.

Ever since I went into menopause I feel like I’m living in a different body…and have a much harder time losing weight…is this the new normal?

Menopause is a new normal for women but it need not be a nightmare! The extent to which you are gaining weight and feeling like a stranger in a strange body, is very often tied to how far your hormones are out of whack. Shifting, declining hormones along with a slowing of metabolism are to be expected at menopause, but their effects are made worse by lack of sleep, chronic stress, and exposure to endocrine disruptors (pesticides, BPA, growth hormones in milk, etc.) in the environment.

At the same time additional burden is placed on the adrenal glands as they take over hormone production from the ovaries at menopause. That can lead to tired adrenals that cannot keep up with demand, so this is prime time to start taking better care of ourselves with improved nutrition, sleep, and stress management. We know that cortisol rises when stress rises, triggering us to refuel by eating more. If stress stays high, blood sugars and insulin will stay high with continued overeating, and inevitably, weight gain. It bears mentioning that the belly fat we women love to hate happens to be the body’s favorite depot for storing energy reserves, which is why doctors often refer to belly fat as the body’s answer to stress.

I think I may be deficient in Vitamin D but I take a multivitamin every day…isn’t that enough?

If you are overweight you will want to make sure that you are not D-deficient, given what researchers are finding is a strong association with increased body fat and obesity onset. The so-called ‘sunshine vitamin’ is actually a ‘prohormone’ made in the body by the action of sunlight upon the skin. So those of us who live in the grayer, northern altitudes are typically low in D, but deficiency occurs even in sunny climates where you would least expect it, attributed to overuse of sunscreens and covering up against the D-enriching rays of the sun. As humans increasingly spend more time indoors in front of computers, and less time working or exercising outside when the sun is shining, the problem is taking on epidemic proportions. Sensible sun exposure, from15 minutes to a half hour a day can help boost D levels as nature intended.

To circle back to your question about supplementation, the amount of D3 contained in the average multivitamin may not be enough to raise D levels into the healthier ranges. If testing your D levels reveals a deficiency (30 ng/ml or below) talk to your provider about increasing your daily D intake. Supplementing between 2000 and 5000IUs of Vitamin D3 is generally suggested to bring levels into the optimal (50-80 ng/ml) range.

Could an imbalance in Estrogen/Progesterone cause low cortisol? I have low cortisol across the board.

This is certainly to be considered, particularly when there is too much estrogen relative to too little progesterone, an all too common imbalance known as estrogen dominance. This often shows up in the test results of women in menopause and perimenopause, when waning ovaries no longer make estrogen and progesterone in balanced proportions. This is also not atypical in younger women on birth control, with anovulatory (lack of ovulation), or erratic cycles.

Progesterone being high up in the hormonal cascade is also a precursor (source) of  primary adrenal hormones, so if it is in short supply, DHEA and cortisol, the key arbiters of adrenal health will also be down with some level of adrenal fatigue to follow. So your question is a good one: imbalances of estrogen and progesterone can and will negatively impact cortisol levels down the line. If you feel this is what’s going on with you consider testing your hormone levels to identify hidden imbalances and work with a provider to restore balance naturally.

If a patient is on birth control pills, can a saliva test be accurate?

Hormones levels tested while ‘under the influence’ of the pill will reflect its’ contraceptive effect and test at lower levels than would be the case in the absence of contraception. To get a true baseline level of hormones, it is suggested that birth control be suspended for four to six weeks before collecting hormone samples. Having said that, women who do test their hormones while taking contraceptives may use the results of testing to guide decision making about hormonal vs. non-hormonal birth control methods.

I am estrogen dominant, taking lots of supplements, I do bioidentical progesterone the last 2 weeks of my cycle; I’m perimenopausal, periods now 6 weeks apart, I have really high cortisol in the morning and in the evening, I do yoga, exercise and all the supplements -what else can I do? 

Sounds like you are doing many things right, but if you still have depression, weight gain, and stress demands high enough to spike your cortisol levels morning and evening, look to your adrenal glands. These master stress responders need extra support especially during perimenopause when hormonal shifts and fluctuations trigger imbalances that can amplify stress demands upon the body.

Supplements like Vitamins C, B-complex, adaptogenic herbs, and natural progesterone, etc., when taken in the right amounts are essential adrenal supports, and the practice of yoga with its stretching and deep breathing is known to help lower stress hormones. All good, but if as you say your cortisol levels are still high, you may have to drill down a bit more and ask yourself how you are dealing with stress. If you’re overworked, overbooked, over-caffeinated, or feeling overwhelmed in general, it’s time to take stock of your stress, figure out where it’s coming from and how you can alleviate it at the source. That may be as simple as turning off your cellphone after 8pm and going to bed earlier, or as complicated as switching careers and walking away from the ‘dream job’ that drained you dry.

Lack of sleep by the way is one of the biggest contributors to cortisol imbalance, and a serious disruptor of appetite hormones, leading to sugar cravings and increased hunger. Getting by on just 5 or 6 hours a night will undermine your best efforts to stay healthy and balanced and a number of studies show that ‘short sleepers’ are more prone to weight gain. Aim for 7 to 8 hours a night at minimum, and “sleep in on the weekends whenever possible,” says Dr. James Wilson in his must read book: Adrenal Fatigue, The 21st Century Syndrome. 

Do you feel saliva over blood tests is better?

If you want to test active bioavailable hormone levels that correlate more closely to the symptoms you are experiencing, saliva testing can be a better way to go. That’s because this method (see also blood spot collection) captures the ‘free’ fraction of hormone that has left the blood stream to become active in the target tissues of the body; in contrast the standard blood test measures inactive hormones still bound by their carrier proteins in the blood stream. Saliva testing has another big advantage: collection is non-invasive, that is without needles, so all one has to do to collect hormone samples is spit into a tube – a painless change from the stress of a blood draw that can skew results.

My doctor did a blood test and said my hormones are fine and that I’m just depressed. Now I’m on Prozac, and gaining more weight!

I have a one-line response to your comment: Depression is NOT a Prozac deficiency. (see question above regarding blood tests.)

What is the call to action?  

In a nutshell; become aware of, and determine your own symptoms of hormone imbalance, test your hormone levels to identify imbalances that match up with the symptoms you are experiencing, and last but not least find a natural hormone friendly provider who will work with you to rebalance your hormones.

A savvy practitioner will test, not guess using hormone test results as a guide to individualizing treatment. After all, each of us has a unique body chemistry, so what works for one woman does not necessarily apply to her friend, sister or next-door neighbor.  Today’s more enlightened and effective approach to a woman’s hormones and weight gain is bound to include lifestyle and dietary improvements, stress lowering techniques, key vitamins, minerals, herbs and/or bioidentical hormones as needed, to replenish and restore balance.

Common hormone-related causes of weight gain often involve the following scenarios:

Estrogen & Progesterone Imbalances

Result in weight gain in hips and thighs, water retention & sluggish metabolismLow Testosterone or DHEA

Lead to decreased lean muscle and increased body fat, decreased metabolic rate & abdominal obesityHigh Cortisol

Results in insomnia, anxiety, sugar cravings, feeling tired but wired & increased belly fatLow Cortisol

Causes chronic fatigue, low energy, food and sugar cravings, poor exercise tolerance or recovery & low immune reservesVitamin D3 deficiency

Associated with hyperinsulinemia & increased belly fatHigh TSH

Leads to hypothyroidism, low metabolic rate & obesityHigh Insulin

Indicative of insulin resistance, metabolic syndrome & abdominal obesityHigh HbA1c

Predictive of type 2 diabetes

Balance Your Hormones to Balance Your Weight

  • Hormones regulate weight, blood sugar, and when and where the body stores fat
  • Hormones are the driving force behind metabolic regulation
  • Estrogen and progesterone promote healthy fat distribution in hips and thighs
  • Testosterone/DHEA support muscle mass and metabolic rate
  • Cortisol regulates sugar control
  • Thyroid regulates metabolism
  • Insulin regulates fat storage

Symptoms of imbalance of hormones:

  • Unexplained weight gain
  • Sluggish metabolism
  • Raging appetite
  • Emotional eating
  • Fatigue and burnout
  • Decreased libido
  • Insomnia
  • Less lean muscle mass
  • High body fat
  • Stress is unresolved

Hormonal Weight Gain in Women

Premenopause: irregular cycles, cravings, premenstrual weight gain

Peri-menopause : erratic ovulation, shifting hormones with onset of symptoms, increased cortisol and belly fat – more stress

Post-menopause: Endof ovulation – leads to imbalances of female thyroid hormones/cortisol

Hormone weight Gain in Men

Men lose testosterone and DHEA  – lean muscle goes and body fat goes away – ratio of estrogen rises and female fat pattern

Slowing of metabolism, feel muscle soreness and exercise less.

What Tips the hormonal balance:

Chronic stress triggers blood sugar and insulin imbalances – weight gain and belly fat in creases

Poor nutrition causes food cravings, weight gain and insulin resistance.

Lack of exercise is linked to overeating, obesity, blood sugar imbalances and loss of lean muscle mass that is replaced by fat

Xeno-estrogens are endocrine disruptors that cause weight gain and hormonal imbalance

Imbalances in hormones are demonstrated by:

  • Estrogen dominance in which weight gain is primarily in the hips, thighs, buttocks, and breast tissue. There is a difficulty in losing weight and maintaining weight with sugar and fat cravings. Slow metabolism with thyroid being low symptoms. Hunger even after you just ate. Estrogen dominance can interfere with the thyroid function
  • Adrenal Imbalance- adrenal makes cortisol to regulate glucose Stress causes cortisol to rise and insulin rises as a result and causes fat deposition. Adrenal fatigue occurs – tired in the morning and wired in the evening.  Results in hunger and cravings – hard wired to be hungry.
  • Causes of adrenal imbalance – chronic stress | Diet high in sugars, carbs, caffeine | Lack of sleep | Midlife

High Cortisol:

  • Increases cravings for sweets and carbs – overeating and constant hunger
  • Breaks down muscle for energy – less lean muscle and lower metabolism
  • Causes more fat in the abdominal area
  • Linked to DEPRESSION – when depressed you eat more

Androgen Imbalance: (testosterone and DHEA)

  • High Testosterone linked to insulin resistance, central obesity, PCOS
  • Lows leads to lean muscle loss and lower metabolism

Thyroid Imbalance:

Adrenal and estrogen imbalance can interfere with thyroid function

Insulin Resistance:

Insulin regulates blood sugar and elevates from high carbs and sugars and eventually gets resistance . Eventually sugars are used to make fat and not for energy: Results in inflammation, metabolic syndrome and Type 2 diabetes.

Vitamin D Deficiency in Weight Gain:

  • Vitamin D is a hormone – low sun exposure and fall in Vitamin D results in Winter metabolism increasing energy stores as fat mass
  • Low vitamin D is associated with insulin resistance and increased waist circumference. Low Vitamin D has 3x more subcutaneous fat and low vitamin D may increase obesity over time.
  • Supplement Vitamin D to get above 30 ng/ml (50-80 ideal)
  • Foods with Vitamin D like fatty fish (salmon and sardines) milk, OJ suggested.

Balance your diet:

  • Organic only to avoid xenohormones, pesticides
  • Whole foods
  • Crucifers: Kale, cabbage, broccoli, Brussel sprouts rid xenoestrogens and xenohormones
  • Low glycemic
  • Low sugar
  • High Fiber
  • Good fats
  • Herbal teas
  • Water

Caffeine raises cortisol and glucose levels

Balance your supplements:

MVI

  • DIM – indoyl methane – in cruciferous vegetables
  • CA, Magnesium
  • Omega 3  – decreases inflammation in the body
  • Vitamin D3
  • B complex
  • Adaptogenic  herbs – Maca, Rhodeola – strengthen the adrenal gland – normalize stress levels to decrease cortisol levels
  • Zinc and selenium – for thyroid hormone

Get sleep – less than 7 hours of sleep increases increased ghrelin and decreased leptin. Lack of sleep disrupts the appetite hormones that operate on the sleep-wake cycle.

Strength and weight training builds lean muscle and increases DHEA and testosterone


Addiction

California Addiction Treatment Data

California’s Treatment Data

In each year between 2007 and 2017, the Pacific division, which includes the State of California has had the largest number of admissions among all Census divisions in the United States, with 403,316 addiction treatment admissions.  This number is primarily based upon the data collected for the Treatment Episode Data Set (TEDS), DEPARTMENT OF HEALTH AND HUMAN SERVICES Substance Abuse and Mental Health Services Administration (SAMHSA).  The data includes publicly funded treatment providers and does not include private treatment facilities that do not report their treatment episode data.   This data set is utilized to describe the picture across the country and in this case the State of California.

California Rehab Reporting

The Numbers

According to TEDS in 2007 treatment facilities across the country saw 2,162,877 treatment episodes 844,544 were for Alcohol and 399,853 for Opiates.  In 2017 treatment admissions dropped to 2,005,395 with 590,681 for Alcohol and 682,074 for Opiates.

State data numbers

The Role of Opioids in the Country

The Opioid epidemic has run rampant for more than a decade now and has brought with it several substantial issues to our countries health, and legal systems. SAMHSA reports that in 2017 there were  533,394 Heroin treatment episodes and when you include Opioid (Heroin and Opiates other than Heroin) there were an additional 148,680 treatment admissions the highest of primary substances, with the second being alcohol (only) at 333,732.

In 2007, 14 percent of admissions aged 12 years or older were for primary heroin use. In 2017,

27 percent of admissions aged 12 years or older were for primary heroin use.  That is nearly double over the course of a decade. These numbers are consistent across the country.

Primary substance use at admission chart

Opiates Other Than Heroin

The proportion of admissions aged 12 years or older for the primary use of opiates other than heroin increased from 5 percent in 2007 to 10 percent in 2011 and 2012, before declining to 7 percent in 2017.  This may be indicative of the trend in the country to use Heroin as it is a cheaper alternative, easier to buy now that the Country has put significant legal pressure on the prescribing physicians, and the awareness of the American Medical Association (AMA) pain policy.

Methamphetamine/Amphetamines

Let’s not forget about the Methamphetamine and Amphetamines treatment episodes as they are not small in number and have certainly not gone away!.  Often we see trends across the country with California treating a significant rate of individuals for Methamphetamine. The proportion of admissions for primary methamphetamine/amphetamines aged 12 years and older ranged between 8 and 12 percent from 2007 to 2017. The average age at admission was 34 years for primary methamphetamine/amphetamine admissions.

Admissions age factors have shifted between 2007 and 2017.

The proportion of admissions aged 12 to 20 years decreased from 14 percent in 2007 to 7 percent in 2017.

The proportion of admissions aged 25 to 34 years increased from 26 percent in 2007 to 35 percent in 2017.

The proportion of admissions aged 50 years and older increased from 11 percent in 2007 to 18 percent in 2017.

State data for age at admission

SOURCES: Center for Behavioral Health Statistics and Quality, Substance Abuse and Mental Health Services Administration, Treatment Episode Data Set (TEDS). Data received through 11.21.18. Population: U.S. Census Bureau, NC-EST2017-ALLDATA: Monthly Population Estimates by Age, Sex, Race, and Hispanic Origin for the United States: April 1, 2010, to July 1, 2017.

Are our Treatment Strategies working?

This seems to indicate that on the surface the countries youth strategies may be effective.  However, a closer look may point to the increased access to treatment for young adults with the “Mental Health Parity and Addiction Equity Act (MHPAEA)” being passed by Congress in 2008. Then followed up with the 2013 Federal rules to implement the law.  Prior to that Insurers, including Medicaid and Medicare policies, limited reimbursement for Behavioral Health including Substance Use Disorder(s).

Reasons for Discharge

California Stands above most States for Health Insurance Regulation

California has been vocal as well as action-oriented about its stance on Parity.  The Federal guidelines state that the Federal rules are the minimum standard and if a State, like in the case of California, has more stringent rules, the State rules prevail.  Fortunately, these Federal rules carry more weight as Insurance has been a near untouchable system throughout the country’s history.

What is Addiction Treatment?

First and foremost, addiction treatment is the treatment of a medical condition classified as a behavioral health condition.  As mentioned earlier behavioral health conditions must be treated by health agencies with the same regard as any other medical condition.  There must be a diagnosis, treatment-specific protocol, and plan. As with any other medical condition, a patient should seek a consultation by a licensed or credential professional in the field of addiction or addiction medicine.

How a Diagnosis is Formed

A diagnosis is determined by utilizing the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, the DSM-5 published by the American Psychiatric Association.  If you are wondering, yes, addiction or the medical term, Substance Use Disorder is a psychiatric illness, recognized worldwide by the World Health Organization. The classification process is called the ICD-10, it is the 10th edition (revision) of the International Statistical Classification of Diseases and Related Health Problems (ICD).

Once diagnosed, an individual would be assessed for appropriateness for a specific level of care.  The American Society of Addiction Medicine (ASAM) has a set of criterion for Substance Use Disorder Treatment.  Contrary to popular belief, addiction treatment or “rehab” is not a 30, 60 or 90-day process.  Addiction treatment or recovery is an as-needed process. An individual must fit the criteria for a specific level of care in order to be treated at that level of care.  For instance, if a patient is seen by a cardiologist for a 50% arterial blockage the treatment would not be a radical quadruple bypass surgical procedure. Correspondingly, addiction treatment is the same.  Of course, it is trickier than a cardiac issue, it is clear to see a physical arterial blockage whereas, Substance Use Disorder relies on self-reporting of symptoms. Often, the individual minimizes their use, thus a poor diagnosis.

What is a Level of Care?

The ASAM Criteria is broken down into six dimensions.

  • Dimension 1: Acute Intoxication and/or Withdrawal Potential
  • Dimension 2: Biomedical Conditions and Complications
  • Dimension 3: Emotional, Behavioral, or Cognitive Conditions and Complications
  • Dimension 4: Readiness to Change
  • Dimension 5: Relapse, Continued Use, or Continued Problem Potential
  • Dimension 6: Recovery and Living Environment

The level of severity from lowest to highest for each dimension is utilized to recommend an appropriate level of care.

ASAM lists the levels of care as:

  • 0.5 Early Intervention
  • 1 Outpatient Services
  • 1 Opioid Treatment Program (OTP Level 1)
  • 2.1 Intensive Outpatient Services
  • 2.5 Partial Hospitalization Services
  • 3.1 Clinically Managed Low-Intensity Residential Services
  • 3.3 Clinically Managed, Population Specific High-Intensity Residential Services
  • 3.5 Clinically Managed High-Intensity Residential Services
  • 3.7 Medically Monitored Intensive Inpatient Services
  • 4 Medically Managed Intensive Inpatient Services

For simplicity the categories would be ambulatory, rehabilitation/residential, detoxification, and medication-assisted opioid therapy.

Level of care at discharge

A skilled, licensed or credentialed clinician assesses the patient via a set of questions, gathering of clinical data and history and then recommends a level of care for treatment.  Furthermore, the patient will move through a continuum of care from one level to another, and at times back due to the regressive nature of the manifestation of the illness. In simple terms, Detox, (withdrawal management), then residential followed by outpatient care.  In response to a physical or emotional relapse, an individual could be recommended a higher level of care in the process of the treatment episode.

The Impact in California, Drug Overdose deaths

The Centers for Disease Control and Prevention (CDC) reports that during the year 2017 there were 70,237 drug overdose deaths, with 47,600 (67.8%) involving opioids.  That is over 130 Opioid overdose deaths a day and over 192 of all drug-related overdose deaths per day! In California, there were 2,196 opioid-related overdose deaths reported, that’s over 6 Opioid overdose deaths per day and a total of in the State.  There are limitations to these numbers to be aware of. First, toxicological tests have improved over the years so autopsies are now more drug-specific.  Additionally, often in the past Medical Examiners would not list all contributing substances on the death certificate. However, the numbers have grown and are clearly impacting our Country and the State of California significantly.

Impact on California

Impact to the Community at Large

On Oct. 26, 2017, President Trump Declared the Opioid Epidemic a Public Health Emergency.  He was quoted as saying, “As Americans, we cannot allow this to continue.” It is clear we face a major issue in the country and California is not exempt.  The State faces significant budget issues as the economy slowly rebounds. Not since the 1980’s HIV/AIDS crisis has the Country faced an issue with greater ramifications.

What is the financial impact?

A 2018 report by Altarum, a nonprofit health research institute, indicates the economic impact exceeds $1 Trillion dollars between 2001 and 2017 and expects an additional half a trillion by 2020.   These numbers take into consideration; lost wages, low productivity in the private sector, health care costs, government spending on and in response to the crisis via health care, social services, and criminal justice expenditures.  Besides the loss of life, quality of life for the individual and families of the affected, and the overall spiritual and emotional damage to the country, Opioids and Substance Use Disorder(s) are ravaging California and the Country.

Discussion

Over more than a decade, the Country has been engulfed in an epidemic of grand proportion. Opioids have taken the country by storm. The effects on California and its population has been devastating. On average six people die every day in California due to Opioid overdose. When you add to that number overdoses from other drugs, motor vehicle casualties due to alcohol and other drug consumption, the health issues associated with drug use, and death by suicide there is no doubt that addiction is playing a huge role in our communities.

Finding solutions to these issues is high on the list for action steps. Substance use disorder treatment is more important today than ever. Addressing prevention and harm reduction are necessary for a full-scale assault on this public health issue. Politics aside representatives from both sides of the aisle and in between must recognize the dilemma we face and come together to find keep our communities, states, and country safe and on a healthy path.

Recovery

7 Simple Steps to Getting Your Life Back on Track in Recovery

7 Simple Steps to Getting Your Life Back on Track in Recovery 

If you’re in recovery, you’re probably looking for other ways to help get your life on track. Contributing to your recovery with simple habits, like exercise, stress-relief and healthy eating, can help you truly thrive as you take back control of your life. Here are some easy changes you can make so you can take charge and continue to heal. 

Make Daily Exercise a Habit  

Exercise is obviously good for your body, but exercise can also be good for your brain. Working out can help you feel more alive by boosting the endorphins your brain produces, which in turn leads to more feelings of happiness and less sensitivity to pain. So find simple ways to get a workout in every single day. Take your dog for a brisk walk or do strength training at home. Even 30 minutes a day is enough to make a significant difference in how you feel physically and mentally. If sleep is an issue, make a point to get your exercise in the morning, which can make it easier to fall off to dreamland at night. 

Get Outside for Some Fresh Air 

Being outside is an incredible way to boost your physical and mental health. Spending just a few minutes in the sun will help your body process and produce essential vitamins for keeping you healthy and strong. Plus, being outside has been proven to have a whole host of health benefits, so find ways to enjoy the outdoors on a regular basis. Have your coffee outside or go for a morning walk, to get some fresh air and fuel your recovery. 

Tackle the Big Stuff

It’s not unusual for individuals in recovery to have serious debt or financial issues waiting for them when they complete treatment. This can be a major stressor that leads to relapse, so it’s important to take the bull by the horns here and map out a plan. If bills are out of control, look for ways to make payment plans or consider debt counseling. You can also find ways to trim expenses and stick to a modest budget. And don’t get caught up in thinking you’re stuck. Maybe your auto insurance rates went sky-high after a DUI or a reckless driving charge, but they don’t have to stay that way. By talking to your provider and taking defensive driving courses, you can help your record and reduce your premiums. 

Start Some New, Exciting Hobbies 

Boredom is a gateway to potential relapse, so why not pick up some new hobbies to keep yourself busy and productive? Try your hand at starting a garden, start painting or learn to play a musical instrument. Looking for something a little more low-key? Then dabble in hobbies that are known for their relaxation properties. Simple hobbies, like knitting, coloring or reading, are good ways to pass the time and keep yourself occupied.

Find Healthy, Positive Ways to Relieve Stress 

Self-care and stress relief are also essential to thriving during and after recovery. Stress can be a major trigger for relapse, and harmful to your overall health. To ensure you don’t turn to harmful stress-relieving activities, look to positive stress relief instead. You can enroll in a weekly local yoga class to bring some calm to your life, or start doing daily meditations. 

Work on Building Positive Bonds With Friends and Family 

Your relationships have a big impact on your health and happiness. Take time to eliminate negative connections from your life, so you can thrive and feel happier. Nurture your positive connections with friends and loved ones by meeting for lunch, coffee or just hanging out. Join some social groups or meetup to find new connections and make it a point to stay social as you move through your recovery. These positive connections can help you stay on track to reach your health goals. 

Eats Lots of Healthy, Fresh Foods 

A healthy diet is another way to keep yourself strong during recovery. Eating the right foods will give you the strength and vitality you need to feel confident and focused. Try preparing meals at home to make sure you’re staying healthy. If you have a hard time staying on track, meal prepping is a great way to stick to your new diet without having to take up too much of your time. 


Taking steps to contribute to your recovery is a wonderful way to thrive and find happiness in your life. With simple daily habits, you can win the fight against addiction and take control of your life. So make these healthy changes today to change your life for the better!

Photo Credit: Pexels


Thank you for your time,
Adam

Adam Cook
Addictionhub.org
information@addictionhub.org

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Suicide is preventable: How can we help our teens?

Every October, after school starts—and each May, as it ends—there is a spike in the number of teenagers who go to the Yale New Haven Children’s Hospital (YNHCH) emergency department because they are thinking about attempting suicide. They may or may not have struggled with a mental health issue before. But they often have a story: Bullies are harassing them, their parents are divorcing, the academic pressure is crushing them. For some, it’s gender concerns—they have come out as trans or non-binary, and their peers are shutting them out.

“It’s everything—all the pitfalls of being a teenager,” says Kirsten A. Bechtel, MD, a Yale Medicine specialist in the YNHCH, where she says 1,500 to 1,700 of the 40,000 patients a year come in for care for anxiety, depression, and other mental health and behavioral problems, and about 500 of those have suicidal thinking or behavior. In some cases, there may be no clear reason at all, she says.

Suicide is preventable, but rates of suicide are increasing worldwide, and it is now the second leading cause of death in adolescents and young adults (unintentional motor vehicle accidents are first).

Going to the emergency room may be the smartest thing these teenagers can do, Dr. Bechtel says. YNHCH is a Level 1 pediatric trauma center and provides subspecialty care for vulnerable children. Even a single attempt, not to mention an actual suicide, is a tragedy, she says, and a sign that there is a need for more prevention.

Why are teen suicides increasing?

Experts aren’t sure why there is an escalation in teen suicides, and an increase in mental illnesses, like depression and bipolar disorder, that are linked to suicide. One potential trigger may be what’s called “contagion”—when one suicide seems to prompt a chain reaction of suicides. Controversy has swirled around the Netflix series “13 Reasons Why,” which highlights the story of a girl who killed herself and left behind tapes to explain why. While some argue that the show has stimulated a positive conversation around the topic, a study in the Journal of the American Academy of Child and Adolescent Psychiatry showed a 28.9 percent increase in suicide rates in young people ages 10 to 17 in the month after the show’s release in April 2017. (In July 2019, producers followed advice from medical experts and cut a scene that portrayed the suicide.)

Social media also comes under discussion. “There is tantalizing data as far as the effects of social media, but I don’t think we have a good grip on that association,” says Yann Poncin, MD, a Yale Child Study Center psychiatrist, and medical director of the Children’s Day Hospital and In-Home Intensive Child & Adolescent Psychiatric Service. Dr. Poncin has noticed that many teenagers with depression—especially girls—turn to the online world. “I think the use of social media in a teenager with pre-existing concerns does fuel the fire a bit,” he says.

Although Dr. Bechtel has seen cases where social media has been used to alert friends that a teenager was in trouble, Facebook and Instagram can also drive a vulnerable teen to despair, she says. “The negative feedback teenagers get about what they said, what they wore, and who they are is so intense,” she says.

However, some of the biggest issues teens face are not new at all, Dr. Poncin says. A common one is loss—a romantic breakup, the end of a friendship, a death or divorce in the family—combined with underlying psychiatric disorders such as anxiety, depression, and bipolar disorder, which are also on the rise. Another is bullying: In a 2008 study, Yale researchers reviewed studies from 13 countries and found a connection between bullying and suicide.

How do you know a teenager is in trouble?

One thing experts agree on is that teenagers look at the world differently than adults do. “Psychologically, teenagers tend to have more absolutist views. They see things in starker, more rigid colors, and they see fewer gray areas,” says Eli Lebowitz, Ph.D., the director of the Program for Anxiety Disorders at the Yale Child Study Center. “This view can make a problem seem more daunting and a solution seem less likely, where a more mature person might be more accustomed to realizing that life has a combination of good and bad.”

Dr. Lebowitz tells parents who are worried to look at the teen’s ability to function. “‘Normal’ is ultimately the ability to function in way that is in line with expectations for someone of a similar age,” he says. For a teenager, that means attendance, performance, and the ability to get along with others at school, he explains. It is having a satisfying social life in and out of school, and the ability to participate in a reasonably functioning family life (whether or not it is devoid of conflict). It includes the “ability to eat, sleep, and get through a day feeling OK,” he says.

Jennifer Dwyer, MD, Ph.D., a psychiatrist at the Yale Child Study Center, says parents should pay attention if their teenager is chronically angry, cranky, or irritable, since teen depression may manifest through these behaviors rather than strictly through sadness or crying. But sadness can be a symptom too, she adds. Parents also should take note if teenagers are isolating themselves from friends, in constant conflict with the family or peers, having mood swings, giving away their belongings, or increasing their use of alcohol and drugs, she says.

Should you ask if they are thinking about suicide?

Suicidal ideation—essentially thinking about suicide—is not uncommon; in fact, most teenagers probably have thoughts, even if they don’t try it, Dr. Lebowitz says. But he says that many parents are hesitant to ask their teenager the direct question: Are you thinking about hurting yourself? “Not asking is usually a mistake. You are not likely to cause suicidal behavior if you ask about it,” he says. If the answer is yes, Dr. Lebowitz says the parent can follow up with additional questions:

  • How often do you think about it?
  • When do you think about it (all the time or only when you are really angry)?
  • Do you want to do it?
  • Do you have a specific plan?

If the teenager answers yes, the parent should seek help, Dr. Lebowitz says. “If the answer to the last two questions is yes, that would show the highest level of risk,” he adds. “Even if the answers to those are no, if a teenager thinks about it often, and not only when they are very angry or frustrated, then seeking help is recommended because it would indicate a high level of distress.”

These questions can also help diffuse the situation, Dr. Lebowitz says. “If you are alone thinking about suicide and you’re not able to talk about it, and nobody is asking you, that puts you at higher risk. If someone asks, even if you don’t like that person, it can reduce that sense of isolation. It’s just a fact in the life of a teenager that when somebody does care, it will reduce the risk,” he says.

Getting treatment to prevent suicide

Treatment for suicidal ideation starts with understanding the underlying concerns. Individual therapy, medication management, and the combination of the two could be appropriate, depending on the circumstances. Medicines that treat depression can often include a selective serotonin reuptake inhibitor (SSRI) such as Prozac or Zoloft. The medication can be combined with cognitive behavioral therapy (CBT), which involves regular meetings with a therapist to explore thoughts, feelings, and behaviors to better manage problems. “You can teach someone to recognize their own thinking patterns,” Dr. Lebowitz says. “It’s not instantaneous. But you can train the brain to recognize that pattern and say, “Oh, I’m falling into my thinking trap.””

“A lot of times the relationship with the therapist you are seeing is a good predictor of how therapy might work,” says Dr. Dwyer. “It should be someone the child and the parents feel comfortable bringing their concerns to, and who the child can stick with even when discussing difficult topics.”

Still, about 40 percent of teenagers fail to respond to medication, and half of that 40 percent don’t respond even when they switch to another medication and add psychotherapy, says Dr. Dwyer. “There aren’t a lot of great guidelines or algorithms after you’ve not had success with two medication trials and a trial of evidence-based psychotherapy,” she says.

Given the seriousness of adolescent treatment-resistant depression and suicide, novel treatments are currently being investigated. Ketamine is an anesthetic that has made headlines for its surprising antidepressant effects in adults. Esketamine, a related compound that is delivered as a nasal spray, was approved by the Food and Drug Administration (FDA) this year for treatment-resistant depression in adults. This medication works rapidly, within 24 hours, to reduce depressive symptoms compared to SSRIs, which take weeks to work. Ketamine is also associated with a reduction in suicidality in adults, even after controlling for any improvements in depressive symptoms.

Ketamine and esketamine are only now beginning to undergo rigorous testing for adolescents with treatment-resistant depression and suicidality. A small randomized clinical trial at Yale showed a positive effect of a single ketamine infusion in adolescents with treatment-resistant depression compared to a placebo, but this study only looked at short-term (two-week) outcomes.

Unfortunately, single doses of ketamine typically do not lead to sustained antidepressant responses, and Dr. Dwyer’s group is now conducting a trial looking at a limited number of repeated ketamine doses (which are associated with prolonged antidepressant effects in adults) in this population. But caution is warranted, Dr. Dwyer says, noting that some animal studies suggest that younger ages may be more susceptible to damage to the brain from a high dose of ketamine. It’s important to realize that ketamine is still considered an experimental treatment at this time for pediatric patients, she emphasizes. “I’m hopeful, but I’m also cautious about it, because I think the issues of effective and safe dosing paradigms in the population still need to be worked out,” says Dr. Dwyer.

What we are learning about the teenage brain

Meanwhile, neuroscientists are looking for clues in the brain which, in teens, is still developing. “Adolescence is a time when suicidal thoughts and behaviors can start to emerge,” says psychiatrist and neuroscientist Hilary Blumberg, MD, director of the Mood Disorders Research Program at Yale School of Medicine. She is using magnetic resonance imaging (MRI) to take pictures of the brains of adolescents and young adults with bipolar disorder who are at especially high risk—an estimated 50 percent of whom will attempt suicide at some point.

“We’re identifying the brain circuitry that underlies suicide thoughts and behaviors, how its trajectory of development differs in adolescents at risk for suicide, and how this can be helped,” says Dr. Blumberg, who has seen subtle variations in the prefrontal cortex of young people who have attempted suicide. (The prefrontal cortex has such executive functions as regulating emotions and impulses, and decision-making and planning. It can be compromised by various kinds of child abuse, substance abuse, and other stressors.) She and her research team have also observed subtle differences in the prefrontal structure in teens who go on to make a suicide attempt. “This provides us with new leads about how to generate targeted interventions to prevent suicide.”

Dr. Blumberg is also studying Social Rhythm Therapy (SRT), an approach that she says is showing early promise for normalizing brain circuitry and preventing suicide. SRT is designed to improve mood by regulating emotions and regularizing daily “rhythms”—an example of the latter is sleep patterns. “In order to help people have more regular sleep, you have to look at potential issues that may be causing the disruption. Their issues could be tied to social interactions and activity throughout the day, and a therapist can help them problem-solve around that,” Dr. Blumberg says. “We are encouraged by preliminary results where, after 12 weeks of regularizing daily rhythms, we see reductions in symptoms and suicide risk, and improvements in related brain circuitry.”

“The field has made important progress, but more research is needed,” Dr. Blumberg says. She is the U.S. lead of an international research consortium studying the brain scans of thousands of young people around the world who have suicidal thoughts and behaviors. She notes that the research is promising and may also turn out to be helpful to people who have bipolar disorder, as well as depression and other mental illnesses. “The future is very hopeful. We already have some strategies to prevent suicide, and it is especially hopeful that researchers from different disciplines are coming together in global efforts to discover new ways to reduce suicide.”

What if you are worried about suicide now?

Of course, many families need help immediately. If this is the case, Maryellen Flaherty-Hewitt, MD, a Yale Medicine pediatrician, recommends talking to the family pediatrician. “We routinely ask questions about access to guns, medications in the home, video games teenagers are using, and if they are exposed to violence,” says Dr. Flaherty-Hewitt. The pediatrician should be alert to teenagers who have had no history of mental illness, but who may be having difficulty coping with, say, feelings about sexuality, bullying at school or online, or the transition from one school to another, she says.

“When you have a child who has suicidal ideation, it’s a crisis, and pediatricians want to be part of this conversation. We want to make sure we bring the right people into the mix right away,” Dr. Flaherty-Hewitt says.

If the crisis warrants going to the emergency room, one of the first things that will happen is a counselor will sit with the teenager and listen to their concerns. In some cases, the patient will be admitted to the hospital or referred to YNHCH’s Partial Hospitalization Program. But, Dr. Bechtel says, “I’m always amazed how some of these kids are alright. Maybe they needed some respite, or maybe the biggest problem is that their behavioral health needs aren’t being met in the community,” she says.

For most young patients, thoughts of suicide are manageable, specialists say. “It may be a lifelong vulnerability, but there are many people who used to have an anxiety disorder or depression,” says Dr. Lebowitz. “We need to foster a belief in treatment and the understanding that having these problems can be part of life.”

Social Rhythm Therapy (SRT)

Magic Medicine?

Patients are turning to ketamine and other psychoactive drugs for mental health treatment

Sarah Jones, a 42-year-old stay-at-home mom in Woodstock, has struggled with depression since childhood. She’s tried multiple antidepressants and therapies over the years, and last fall, her medications once again quit working. Then Jones heard a radio ad about a new approach for depression — a drug called ketamine.

Ketamine is an anesthetic commonly used by veterinarians. It’s also used illegally as a club drug for its mind-altering, euphoric effects. And recently, it’s been touted for a new use: treating depression. 

Other psychoactive drugs like Ecstasy, LSD and magic mushrooms are also being considered as treatments for mental illnesses. Some of the drugs are under consideration for approval by the Food and Drug Administration (FDA).

Ketamine goes mainstream

Over the past several years, ketamine clinics, which deliver the drug to patients through intravenous (IV) infusions, have sprung up in Chicago and around the country to treat depression and other mental health conditions, including post-traumatic stress disorder (PTSD) and anxiety. 

Using the drug this way is considered an off-label use, meaning it’s used in a manner different from what’s been specified by the FDA. IV ketamine treatments for depression are not approved by the FDA and are often pricey. They are typically not covered by insurance. 

In March 2019, the FDA approved a nasal-spray version of ketamine, called esketamine (marketed as Spravato), to help the estimated 5 million Americans whose depression hasn’t responded to other treatments. Research shows that ketamine can more rapidly turn around depression than traditional antidepressants. Suicidal patients can find their urge to harm themselves quelled within 24 hours, rather than the weeks or months it takes a drug like Prozac to take effect, researchers have found.

It’s a bold move by the FDA to approve a completely new class of antidepressants and to open up a new realm of drugs that are considered psychedelics and psychoactive to be used as a medical treatment for something as common as depression,” says Bal Nandra, MD, an anesthesiologist and founder of IV Solution, which for almost three years has provided IV ketamine in downtown Chicago. 

Nandra hasn’t decided whether to offer the recently FDA-approved esketamine nasal spray in addition to IV ketamine. “It’s not nearly as effective or rapid acting as IV ketamine,” he says.

Lifting depression 

Jones received IV infusions of ketamine at Nandra’s South Dearborn Street clinic in November 2018. She followed Nandra’s typical regimen of six treatments given over a period of about two weeks, at a price of $500 to $600 per infusion. 

During these sessions, patients are seated in a private room, where they are hooked up to an IV for about 45 minutes, usually reclining on a medical lounge chair with the room darkened. Often, they wear an eye mask and listen to music. Patients are monitored by nurses or other staff for side effects, and those who become anxious may receive some sedation. After the infusion is over, patients are observed for about 30 to 45 minutes before being released. 

Ketamine can cause patients to feel dissociated from their bodies. The experience left Jones with a sense of the vastness of the universe and the idea that “there is something more out there than what we experience in our everyday life,” she says. “It almost takes you away from your suffering.” 

Most patients feel better after the first few ketamine infusions, Nandra says, though some take longer. Jones felt her depression lifting after her first treatment.  

It’s a bold move by the FDA … to open up a new realm of drugs that are considered psychedelics and psychoactive to be used as a medical treatment for something as common as depression.”

Jones returns to IV Solution every two months for one-session booster infusions to keep her depression at bay. 

She has been able to dramatically reduce her antidepressant use, while continuing in therapy. 

“Ketamine not only restored my brain to being able to function but also gave me insight into some life choices that were adding to my depression,” Jones says. Today, she adds, 

“I don’t remember what depression feels like. I’m so happy!” 

Gregory Teas, MD, a psychiatrist with the AMITA Health Behavioral Medicine Institute, says the clinic will likely start offering esketamine treatment starting this fall. Esketamine has a wholesale cost of $590 to $885 per dose, but the treatment may be covered by insurance, Teas says. Patients can’t take it at home but must go to a medical facility, where it is given under strict protocols, including two hours of monitoring afterward. 

Like other experts, Teas cautions that long-term studies on the use of ketamine and esketamine are needed. While the drug primarily works on receptors in the brain’s glutamate system, it also uses opioid and dopamine pathways, he says, which means it could be addictive for some patients.

Exploring other possibilities

Other psychoactive drugs may soon join ketamine as treatments for psychiatric conditions. The University of Chicago’s Human Behavioral Pharmacology Laboratory, directed by Harriet de Wit, PhD, has been studying MDMA (also known as Ecstasy) as a possible treatment.

MDMA, which causes people to feel loving toward themselves and others, may be helpful for people with PTSD and autism-related social anxiety, says researcher Anya Bershad, MD, PhD, who recently left the lab to complete a psychiatry residency at the University of California Los Angeles. 

A national phase 3 clinical trial of MDMA used in conjunction with psychotherapy for PTSD is underway, though Chicago is not a study site. If these trials go well, researchers expect the FDA might approve MDMA in 2021 for use with psychotherapy as a treatment for PTSD. 

Also being studied at the University of Chicago: microdosing with LSD to treat depression and anxiety. Study participants receive one-tenth or one-twentieth of a recreational dose, usually every three days, Bershad says. They don’t experience mind-altering psychedelic effects, but they do report feeling the “experience of unity,” even at those tiny doses, she says.

Other labs outside Illinois are studying psilocybin, or magic mushrooms, for their potential in treating anxiety, depression and eating disorders. Medical marijuana is also being researched for the treatment of PTSD, though studies differ so far on its effectiveness. 

As for ketamine, Nandra says in the years he’s been offering IV ketamine treatments he has seen many patients recover. “For these people, it lasts,” he says. “They do great. Their lives completely change. … It’s pretty amazing.”

Citocholine for Brain Health

Behind the Buzz: How Ketamine Changes the Depressed Patient’s Brain

The anesthetic-cum-party drug restores the ability to make connections among brain cells

The Food and Drug Administration’s approval in March of a depression treatment based on ketamine generated headlines, in part, because the drug represents a completely new approach for dealing with a condition the World Health Organization has labeled the leading cause of disability worldwide. The FDA’s approval marks the first genuinely new type of psychiatric drug—for any condition—to be brought to market in more than 30 years.

Although better known as a party drug, the anesthetic ketamine has spurred excitement in psychiatry for almost 20 years, since researchers first showed that it alleviated depression in a matter of hours. The rapid reversal of symptoms contrasted sharply with the existing set of antidepressants, which take weeks to begin working. Subsequent studies have shown ketamine works for patients who have failed to respond to multiple other treatments, and so are deemed “treatment-resistant.”

Despite this excitement, researchers still don’t know exactly how ketamine exerts its effects. A leading theory proposes that it stimulates regrowth of synapses (connections between neurons), effectively rewiring the brain. Researchers have seen these effects in animals’ brains, but the exact details and timing are elusive.

new study, from a team led by neuroscientist and psychiatrist Conor Liston at Weill Cornell Medicine, has confirmed that synapse growth is involved, but not in the way many researchers were expecting. Using cutting-edge technology to visualize and manipulate the brains of stressed mice, the study reveals how ketamine first induces changes in brain circuit function, improving “depressed” mice’s behavior within three hours, and only later stimulating regrowth of synapses.

As well as shedding new light on the biology underlying depression, the work suggests new avenues for exploring how to sustain antidepressant effects over the long term. “It’s a remarkable engineering feat, where they were able to visualize changes in neural circuits over time, corresponding with behavioral effects of ketamine,” says Carlos Zarate, chief of the Experimental Therapeutics and Pathophysiology Branch at the National Institute of Mental Health, who was not involved in the study. “This work will likely set a path for what treatments should be doing before we move them into the clinic.”

Another reason ketamine has researchers excited is that it works differently than existing antidepressants. Rather than affecting one of the “monoamine” neurotransmitters (serotonin, norepinephrine and dopamine), as standard antidepressants do, it acts on glutamate, the most common chemical messenger in the brain. Glutamate plays an important role in the changes synapses undergo in response to experiences that underlie learning and memory. That is why researchers suspected such “neuroplasticity” would lie at the heart of ketamine’s antidepressant effects.

Ketamine’s main drawback is its side effects, which include out-of-body experiences, addiction and bladder problems. It is also not a “cure.” The majority of recipients who have severe, difficult-to-treat depression will ultimately relapse. A course of multiple doses typically wears off within a few weeks to months. Little is known about the biology underlying depressive states, remission and relapse. “A big question in the field concerns the mechanisms that mediate transitions between depression states over time,” Liston says. “We were trying to get a better handle on that in the hopes we might be able to figure out better ways of preventing depression and sustaining recovery.”

Chronic stress depletes synapses in certain brain regions, notably the medial prefrontal cortex (mPFC), an area implicated in multiple aspects of depression. Mice subjected to stress display depressionlike behaviors, and with antidepressant treatment, they often improve. In the new study, the researchers used light microscopes to observe tiny structures called spines located on dendrites (a neuron’s “input” wires) in the mPFC of stressed mice. Spines play a key role because they form synapses if they survive for more than a few days.

For the experiment, some mice became stressed when repeatedly restrained, others became so after they were administered the stress hormone corticosterone. “That’s a strength of this study,” says neuroscientist Anna Beyeler, of the University of Bordeaux, France, who was not involved in the work, but wrote an accompanying commentary article in Science. “If you’re able to observe the same effects in two different models, this really strengthens the findings.” The team first observed the effects of subjecting mice to stress for 21 days, confirming that this resulted in lost spines. The losses were not random, but clustered on certain dendrite branches, suggesting the damage targets specific brain circuits.

The researchers then looked a day after administering ketamine and found that the number of spines increased. Just over half appeared in the same location as spines that were previously lost, suggesting a partial reversal of stress-induced damage. Depressionlike behaviors caused by the stress also improved. The team measured brain circuit function in the mPFC, also impaired by stress, by calculating the degree to which activity in cells was coordinated, a measure researchers term “functional connectivity.” This too improved with ketamine.

When the team looked closely at the timing of all this, they found that improvements in behavior and circuit function both occurred within three hours, but new spines were not seen until 12 to 24 hours after treatment. This suggests that the formation of new synapses is a consequence, rather than cause, of improved circuit function. Yet they also saw that mice who regrew more spines after treatment performed better two to seven days later. “These findings suggest that increased ensemble activity contributes to the rapid effects of ketamine, while increased spine formation contributes to the sustained antidepressant actions of ketamine,” says neuroscientist Ronald Duman, of the Yale School of Medicine, who was not involved in the study. Although the molecular details of what happens in the first hours are not yet fully understood, it seems a restoration of coordinated circuit activity occurs first; this is then entrenched by neuroplasticity effects in synapses, which then maintain behavioral benefits over time.

To prove that new synapses were a cause of antidepressant effects, rather than just coinciding with the improved behaviors, the team used a newly developed optogenetic technique, which allowed them to eliminate newly formed spines using light. Optogenetics works by introducing viruses that genetically target cells, causing them to produce light-sensitive proteins. In this case, the protein is expressed in newly formed synapses, and exposure to blue light causes the synapse to collapse. The researchers found that eliminating newly formed synapses in ketamine-treated mice abolished some of the drug’s positive effects, two days after treatment, confirming that new synapses are needed to maintain benefits. “Many mechanisms are surely involved in determining why some people relapse and some don’t,” Liston says, “ but we think our work shows that one of those involves the durability of these new synapses that form.”

And Liston adds: “Our findings open up new avenues for research, suggesting that interventions aimed at enhancing the survival of these new synapses might be useful for extending ketamine’s antidepressant effects.” The implication is that targeting newly formed spines might be useful for maintaining remission after ketamine treatment. “This is a great question and one the field has been considering,” Duman says. “This could include other drugs that target stabilization of spines, or behavioral therapies designed to engage the new synapses and circuits, thereby strengthening them.”

The study used three behavioral tests: one involving exploration, a second a struggle to escape, and a third an assessment of how keen the mice are on a sugar solution. This last test is designed to measure anhedonia—a symptom of depression in which the ability to experience pleasure is lost. This test was unaffected by deleting newly formed spines, suggesting that the formation of new synapses in the mPFC is important for some symptoms, such as apathy, but not others (anhedonia)—and that different aspects of depression involve a variety of brain circuits.

These results could relate to a study published last year that found activity in another brain region, the lateral habenula, is crucially involved in anhedonia, and injecting ketamine directly into this region improves anhedonia-related behavior in mice. “We’re slowly identifying specific regions associated with specific behaviors,” Beyeler says. “The factors leading to depression might be different depending on the individual, so these different models might provide information regarding the causes of depression.”

One caveat is that the study looked at only a single dose, rather than the multiple doses involved in a course of human treatment, Zarate says. After weeks of repeated treatments, might the spines remain, despite a relapse, or might they dwindle, despite the mice still doing well? “Ongoing effects with repeated administration, we don’t know,” Zarate says. “Some of that work will start taking off now, and we’ll learn a lot more.” Of course, the main caution is that stressed mice are quite far from humans with depression. “There’s no real way to measure synaptic plasticity in people, so it’s going to be hard to confirm these findings in humans,” Beyeler says.

Default Mode Network and Mood

The Default Mode Network (sometimes called simply the default network or the DMN) refers to an interconnected group of brain structures that are hypothesized to be part of a functional system. The DMN includes areas of the brain which researchers found to have higher activity when the mind was supposed to be at rest.  For example, when you are day dreaming, thinking about the future, replaying memories, etc. without a specific goal in mind.  Now, why would we care about this? The DMN is found to have increased activity in certain mood and pain disorders.  That being said, let’s look at our 3 reasons why you should know about the DMN. 

Reason #1: Increased DMN activity and functional connectivity is found in depression [1] as well as in pain disorders [2]. In these disorders, there is much rumination.  Rumination is where you have repetitive thoughts.  Those who deal with depression may replay depressing or sad memories over and over in their mind.  This prevents them from healing and creating room for more positive emotions and memories.  Additionally, those with pain may become fixated on the pain itself, or replay the events which lead to them having the pain.  This type of circular, overactive thinking occurs in the DMN. 

Reason #2:  Reducing activity in the DMN can decrease rumination, which in turn can reduce pain and depressed feelings.  In experienced meditators, there was decreased activity in the DMN, as well as increased connectivity in the regions of the brain responsible for self-monitoring and cognitive control [3]. Thus, giving us a scientific reason for the benefits of meditation.  We all have moments where we have unhelpful replays in our minds, and meditation can help us in breaking and reducing this ruminative behavior. 

Reason #3:  Ketamine reduces the functional activity in the DMN! A study showed that the connectivity of the DMN along with another portion of the brain, the dorsal nexus, was decreased after ketamine infusions [4]. So ketamine can effectively turn down the overactive areas in our mind, which can lead to an improved mood and less pain. 

In conclusion, you are much more than your mind, and before you can transcend something which does not serve you, you must know about it. Now that you know more about the default mode network, how your brain works, and rumination, what action will you take today

References:

  1. Hamilton, J. Paul, et al. “Default-Mode and Task-Positive Network Activity in Major Depressive Disorder: Implications for Adaptive and Maladaptive Rumination.” Biological Psychiatry, vol. 70, no. 4, 2011, pp. 327–333., doi:10.1016/j.biopsych.2011.02.003.
  2. Kucyi, A., et al. “Enhanced Medial Prefrontal-Default Mode Network Functional Connectivity in Chronic Pain and Its Association with Pain Rumination.” Journal of Neuroscience, vol. 34, no. 11, 2014, pp. 3969–3975., doi:10.1523/jneurosci.5055-13.2014.
  3. Brewer, J. A., et al. “Meditation Experience Is Associated with Differences in Default Mode Network Activity and Connectivity.” Proceedings of the National Academy of Sciences, vol. 108, no. 50, 2011, pp. 20254–20259., doi:10.1073/pnas.1112029108.
  4. Scheidegger, Milan et al. “Ketamine Decreases Resting State Functional Network Connectivity in Healthy Subjects: Implications for Antidepressant Drug Action.” Ed. Stefano L. Sensi. PLoS ONE 7.9 (2012): e44799. PMC. Web. 23 June 2018.
  5. Sheline, Yvette I., et al. “The Default Mode Network and Self-Referential Processes in Depression.” Proceedings of the National Academy of Sciences, vol. 106, no. 6, 2009, pp. 1942–1947., doi:10.1073/pnas.0812686106.
  6. “Know Your Brain: Default Mode Network.” Neuroscientifically Challenged, 16 June 2015, www.neuroscientificallychallenged.com/blog/know-your-brain-default-mode-network.

NEUROGENESIS

When you break the word itself down, it comes in two parts: “neuro” as in neuron, and “genesis” as in creation. Neurogenesis broadly speaking is the process by which new neurons are created in the brain, thus allowing for increased plasticity of the brain and stronger synaptic connections. Adult neurogenesis is the process by which new neurons are created and integrated into existing brain circuitry when you are an adult. Adult neurogenesis can be seen in the olfactory bulb and the hippocampus.

The hippocampus is an S-shaped structure within the medial part of the temporal lobe and is densely packed with neurons. It a part of the limbic system, which also includes the hypothalamus and the amygdala. This region helps regulate emotion, memory, and arousal. Furthemore, the hippocampus is of particular interest because of its role in learning and motivation.

The monoamine hypothesis of depression states that antidepressants, a.k.a. selective serotonin reuptake inhibitors (SSRIs), work by increasing the levels of serotonin in the brain. It is thought that because SSRIs act on monoamine systems in the brain, which are involved in regulating emotion, therefore antidepressant results will be produced in individuals with depression.

However, treatment using SSRIs often take weeks to months to produce antidepressant effects, and sometimes they’re not even produced at all. People who have difficulty treating their depression with standard medical treatments are described as having treatment-resistant depression (TRD). Researchers are constantly working to find the mechanisms of depression and how it works in the brain.

Published in Neuropsychopharmacology in 2015, Hill and colleagues conducted a study on mice to measure whether inducing adult neurogenesis in the hippocampus positively affects anxious and depressive behaviors. Studies like these are often administered to mice first because they share similar biological and behavioral components to that of humans.

They found that when the mice were treated chronically with corticosterone (stress hormone secreted by the adrenal glands), increasing adult neurogenesis in the hippocampus does reduce anxiety and depression (1).

When we take these findings and circle back to ketamine, it makes sense. One of ketamine’s main mechanisms is increasing neurogenesis and synaptogenesis, allowing for neuroplasticity. Synaptogenesis is the process by which synaptic connections between the neurons in the brain are created. Increasing neuroplasticity allows for the brain to reorganize its connections more efficiently in response to stress and new changes in its environment. Essentially it is what keeps the brain resilient.

So ketamine increases neurogenesis, but why does it have the reputation of being a fast-acting antidepressant, especially for those with TRD? While we don’t have all of the answers to ketamine’s mechanisms, we do know this:

Ketamine Rapidly enhances the Maturation of Neurons

RATHER THAN INCREASING SEROTONIN, KETAMINE ACTS ON THE N-METHYL-D-ASPARTATE (NMDA) RECEPTOR AND THE GLUTAMATE NEUROTRANSMITTER

Ketamine increases the production of Brain Derived Neurotrophic Factor

Ketamine reduces the functional activity of the Default Mode Network

Beyond these multiple mechanisms of action, we also believe there is another level beyond the physical. Accordingly, we incorporate the bio-psycho-social-spiritual model of medicine at our clinic to take a holistic view for our patients!


References:

  1. Hill, A. S., Sahay, A., & Hen, R. (2015). Increasing Adult Hippocampal Neurogenesis is Sufficient to Reduce Anxiety and Depression-Like Behaviors. Neuropsychopharmacology, 40(10), 2368–2378. doi: 10.1038/npp.2015.85

Researchers hypothesize that neurogenesis, or neuron growth, is an antidepressant action. This hypothesis is linked to the understanding that nearly all antidepressants increase birth of granule neurons in rodents. Ketamine, however, has such rapid antidepressant effects, suggesting that the mechanisms involved with ketamine are not involved with neuron birth. Instead, researchers hypothesized that ketamine’s rapid effects are due to it enhancing the maturation of neurons born previously.

To test this hypothesis, researchers injected rats with ketamine, assessing the effects of the ketamine on granule neurons. Researchers found that the ketamine rapidly affected the neurons, increasing mature neurons within two hours. A single injection of ketamine increased cell proliferation and functional maturation. For at least four weeks following the injection, depressive symptoms in rats were decreased.

In conclusion, ketamine has rapid, lasting effects on the recruitment of neurons into the hippocampal region of the brain. The hippocampus is believed to play a role in memory, spacial recognition, and avoidance-approach conflict processing. However, new neuron growth was independent of the antidepressant effects of the ketamine. The antidepressant effect may be due to ketamine’s work on neuron growth, but not on new neuron growth.

epression is among the most disabling conditions in our society. According to the World Health Organization, depression is the leading cause of ill health and disability worldwide. In America, 12.5% of individuals over the age of 12 have filled an antidepressant prescription.  Yet, the effectiveness of these medications are still lacking. Many patients don’t respond to antidepressant medications, and it can take months for the medicine to kick in. Unfortunately, many patients will regain their depression after being on medications long term.

Over 50 years ago, the hypothesis that low concentrations of serotonin in the central nervous caused depression was proposed.  This appealed to many doctors & scientists, because we finally had a potential biological mechanism to explain depression.  Accordingly, many antidepressants were developed to increase serotonin to help relieve depression. Although, it can work for some patients many patients do not respond or have significant side effects.  

SO WHAT IS A PERSON TO DO IF THEY HAVE TREATMENT-RESISTANT DEPRESSION?  

One cutting-edge option is targeting a completely different neurotransmitter – GLUTAMATE. Glutamate is an excitatory neurotransmitter and the most abundant neurotransmitter in the brain and central nervous system.  Ketamine works on the glutamate system by blocking it’s activity at the N-Methyl-D-Aspartate (NMDA) receptor.  

Ketamine raises brain derived neurotrophic factor (BDNF) levels, thereby enhancing connections between neurons and increasing neuroplasticity.  It’s literally changing the brain. In animal studies, the cascade of effects from ketamine created a rapid proliferation of dendritic spines that was associated with less depression. In a functional MRI brain study of humans, ketamine seemed to restore the functional connectivity in those patients with depression. 

Interestingly, ketamine is known to affect other receptors beyond the NMDA receptor, and have  anti-inflammatory as well as epigenetic effects. Also, the breakdown products of ketamine, like (S)-norketamine and (2R, 6R)-hydroxynorketamine, may also play a role in helping with depression. 

Even though we have some understanding of how ketamine works, we still don’t fully comprehend how ketamine is working exactly in patients with depression. 

“We live on an island surrounded by a sea of ignorance. As our island of knowledge grows, so does the shore of our ignorance.

— John A. Wheeler, Physicist

As we continue to learn more about ketamine and depression, more questions and unknowns will surely develop.

Therefore, it’s critical to expand our understanding of depression beyond the simple serotonin and even glutamate neurotransmitters.  The human body, brain, and consciousness is one of the most complex systems we have ever encountered. Although, we may never fully understand the intricacy of it all, we can still take action. 

We can be pragmatic and responsibly use ketamine for carefully selected patients. In addition to ketamine infusions, we can encourage psychotherapy, exercise, meditation, prayer, positive community, a good night’s rest, and a healthy diet to help people with depression.  

At Reset Ketamine, we utilize the bio-psycho-social-spiritual model that encompasses a whole person approach to health.  We believe health is not merely the absence of illness, but a state of physical, social, mental, and spiritual well-being.  We believe ketamine can be the catalyst to create paradigm shifts to help patients live a full life.

References:

Krystal, J. H., Abdallah, C. G., Sanacora, G., Charney, D. S., & Duman, R. S. (2019). Ketamine: A Paradigm Shift for Depression Research and Treatment. Neuron, 101(5), 774-778. doi:10.1016/j.neuron.2019.02.005

ccording to the World Health Organization, depression has now surpassed HIV, AIDS, malaria, diabetes, and war as the leading cause of disability. Current antidepressants may take weeks to months to be effective. Unfortunately, one-third of patients are still unresponsive, and are called “treatment-resistant.” However, there are other options available.

Ketamine, possibly the most widely used anesthetic agent in the world, has been shown by numerous studies to have rapid antidepressant effects when used off-label. The full mechanism by which ketamine induces these therapeutic effects is still a mystery. What researchers do understand is that increased levels of brain derived neurotrophic factor (BDNF), a protein that plays a role in the growth and maintenance of neurons, is involved. But how and where does ketamine increase BDNF?

A recent study in 2017 suggests that HDAC5, an enzyme affecting DNA and chromosomes, regulates the antidepressant effects of ketamine through a process called phosphorylation, which regulates protein function. Ketamine influences the transcription (the process by which DNA is turned into RNA) of BDNF and increases BDNF levels in the central nervous system.

Additionally, a study in 2015 demonstrated that the antidepressant effects of ketamine are based on the release of BDNF and the activation of the L-type voltage-dependent calcium channels (VDCC). Researchers found that the release of BDNF regulates the antidepressant effects of ketamine, further clarifying the underlying mechanisms that ketamine utilizes.

Furthermore, researchers observed in another 2015 study that dysfunctional levels of BDNF may be linked to depression, and that ketamine treatment can produce a positive effect within certain pathways of the brain, such as in the prefrontal cortex and nucleus accumbens. In this animal study, rats were divided into four groups: saline+deprived, saline+non-deprived, ketamine+deprived, and ketamine+non-deprived. Ketamine infusions were administered daily for 14 days. Researchers then observed the animals’ brain structures. They observed that the deprived rats had reduced levels of BDNF in the amygdala, hippocampus and nucleus accumbens. The ketamine reversed the levels of BDNF in the amygdala and nucleus accumbens. This is important because the amygdala plays a critical response in fear and strong emotions, while the nucleus accumbens is essential in motivation, aversion, reward, and learning.

In addition to ketamine’s effect on the default mode network, neurons, brain waves, glutamate neurotransmitter, and inflammation, by understanding ketamine’s impact on BDNF, we can gain a deeper insight into the mystery of how our brain works. Ultimately, as Socrates once said, “To know thyself is the beginning of wisdom.”

References:

Choi, Miyeon, et al. “Ketamine Induces Brain-Derived Neurotrophic Factor Expression via Phosphorylation of Histone Deacetylase 5 in Rats.” Biochemical and Biophysical Research Communications, vol. 489, no. 4, 2017, pp. 420–425., doi:10.1016/j.bbrc.2017.05.157.

Lepack, A. E., et al. “BDNF Release Is Required for the Behavioral Actions of Ketamine.” International Journal of Neuropsychopharmacology, vol. 18, no. 1, 2014, doi:10.1093/ijnp/pyu033.

Réus, Gislaine, et al. “Ketamine Treatment Partly Reverses Alterations in Brain Derived- Neurotrophic Factor, Oxidative Stress and Energy Metabolism Parameters Induced by an Animal Model of Depression.” Current Neurovascular Research, vol. 12, no. 1, 2015, pp. 73–84., doi:10.2174/1567202612666150122122924.

Depression is among the most disabling conditions in our society. According to the World Health Organization, depression is the leading cause of ill health and disability worldwide. In America, 12.5% of individuals over the age of 12 have filled an antidepressant prescription.  Yet, the effectiveness of these medications are still lacking. Many patients don’t respond to antidepressant medications, and it can take months for the medicine to kick in. Unfortunately, many patients will regain their depression after being on medications long term.

Over 50 years ago, the hypothesis that low concentrations of serotonin in the central nervous caused depression was proposed.  This appealed to many doctors & scientists, because we finally had a potential biological mechanism to explain depression.  Accordingly, many antidepressants were developed to increase serotonin to help relieve depression. Although, it can work for some patients many patients do not respond or have significant side effects.  

SO WHAT IS A PERSON TO DO IF THEY HAVE TREATMENT-RESISTANT DEPRESSION?  

One cutting-edge option is targeting a completely different neurotransmitter – GLUTAMATE. Glutamate is an excitatory neurotransmitter and the most abundant neurotransmitter in the brain and central nervous system.  Ketamine works on the glutamate system by blocking it’s activity at the N-Methyl-D-Aspartate (NMDA) receptor.  

Ketamine raises brain derived neurotrophic factor (BDNF) levels, thereby enhancing connections between neurons and increasing neuroplasticity.  It’s literally changing the brain. In animal studies, the cascade of effects from ketamine created a rapid proliferation of dendritic spines that was associated with less depression. In a functional MRI brain study of humans, ketamine seemed to restore the functional connectivity in those patients with depression. 

Interestingly, ketamine is known to affect other receptors beyond the NMDA receptor, and have  anti-inflammatory as well as epigenetic effects. Also, the breakdown products of ketamine, like (S)-norketamine and (2R, 6R)-hydroxynorketamine, may also play a role in helping with depression. 

Even though we have some understanding of how ketamine works, we still don’t fully comprehend how ketamine is working exactly in patients with depression. 

“We live on an island surrounded by a sea of ignorance. As our island of knowledge grows, so does the shore of our ignorance.

— John A. Wheeler, Physicist

As we continue to learn more about ketamine and depression, more questions and unknowns will surely develop.

Therefore, it’s critical to expand our understanding of depression beyond the simple serotonin and even glutamate neurotransmitters.  The human body, brain, and consciousness is one of the most complex systems we have ever encountered. Although, we may never fully understand the intricacy of it all, we can still take action. 

We can be pragmatic and responsibly use ketamine for carefully selected patients. In addition to ketamine infusions, we can encourage psychotherapy, exercise, meditation, prayer, positive community, a good night’s rest, and a healthy diet to help people with depression.  

At Reset Ketamine, we utilize the bio-psycho-social-spiritual model that encompasses a whole person approach to health.  We believe health is not merely the absence of illness, but a state of physical, social, mental, and spiritual well-being.  We believe ketamine can be the catalyst to create paradigm shifts to help patients live a full life.

References:

Krystal, J. H., Abdallah, C. G., Sanacora, G., Charney, D. S., & Duman, R. S. (2019). Ketamine: A Paradigm Shift for Depression Research and Treatment. Neuron, 101(5), 774-778. doi:10.1016/j.neuron.2019.02.005

Researchers hypothesize that neurogenesis, or neuron growth, is an antidepressant action. This hypothesis is linked to the understanding that nearly all antidepressants increase birth of granule neurons in rodents. Ketamine, however, has such rapid antidepressant effects, suggesting that the mechanisms involved with ketamine are not involved with neuron birth. Instead, researchers hypothesized that ketamine’s rapid effects are due to it enhancing the maturation of neurons born previously.

To test this hypothesis, researchers injected rats with ketamine, assessing the effects of the ketamine on granule neurons. Researchers found that the ketamine rapidly affected the neurons, increasing mature neurons within two hours. A single injection of ketamine increased cell proliferation and functional maturation. For at least four weeks following the injection, depressive symptoms in rats were decreased.

In conclusion, ketamine has rapid, lasting effects on the recruitment of neurons into the hippocampal region of the brain. The hippocampus is believed to play a role in memory, spacial recognition, and avoidance-approach conflict processing. However, new neuron growth was independent of the antidepressant effects of the ketamine. The antidepressant effect may be due to ketamine’s work on neuron growth, but not on new neuron growth.


THETA BRAIN WAVES & THE ANTI-ANXIETY EFFECTS OF KETAMINE

According to a study published in the International Journal of Neuropsychopharmacology in 2018, specific brain waves are related to the anti-anxiety effects of ketamine. The brain waves involved in this function are called theta waves, found in the right frontal area of the brain. Ketamine can treat a wide variety of neurotic disorders, such as depression, generalized anxiety disorder, and PTSD, but researchers do not conclusively understand how ketamine works to relieve the symptoms of these disorders.

To better understand the therapeutic effects of ketamine, researchers studied the brain activity of patients given ketamine. Patients with generalized anxiety disorder and/or social anxiety disorder were administered ketamine and hooked up to a monitor measuring electrical brain activity (EEG). Ketamine affected the power of the brain waves by increasing the fast waves and decreasing the slow waves. However, only a single frequency band was related to therapeutic effects—the theta waves.

Human consciousness is believed to be related to neurons firing synchronously in various frequencies. Theta waves are in the 4 to 7 hertz rhythms. During meditation, theta waves predominated and were most abundant in the frontal and middle parts of the brain. Professor Jim Lagopoulos states, “These types of waves likely originate from a relaxed attention that monitors our inner experiences. Here lies a significant difference between meditation and relaxing without any specific technique. Previous studies have shown that theta waves indicate deep relaxation and occur more frequently in highly experienced meditation practitioners. When we measure mental calm, these regions signal to lower parts of the brain, inducing the physical relaxation response that occurs during meditation.”

So ketamine infusions seems to put the brain into a similar state that highly experienced meditators can achieve allowing for a calm, relaxed state of mind.

In conclusion, the anti-anxiety relief of ketamine may related to a very specific portion of electrical brain activity. This finding combined with the knowledge that ketamine blocks the NMDA glutamate receptor helps researchers understand how ketamine affects the brain. This preliminary study paves the way for future research on brain studies and ketamine.

Ketamines impact on BDNF

According to the World Health Organization, depression has now surpassed HIV, AIDS, malaria, diabetes, and war as the leading cause of disability. Current antidepressants may take weeks to months to be effective. Unfortunately, one-third of patients are still unresponsive, and are called “treatment-resistant.” However, there are other options available.

Ketamine, possibly the most widely used anesthetic agent in the world, has been shown by numerous studies to have rapid antidepressant effects when used off-label. The full mechanism by which ketamine induces these therapeutic effects is still a mystery. What researchers do understand is that increased levels of brain derived neurotrophic factor (BDNF), a protein that plays a role in the growth and maintenance of neurons, is involved. But how and where does ketamine increase BDNF?

A recent study in 2017 suggests that HDAC5, an enzyme affecting DNA and chromosomes, regulates the antidepressant effects of ketamine through a process called phosphorylation, which regulates protein function. Ketamine influences the transcription (the process by which DNA is turned into RNA) of BDNF and increases BDNF levels in the central nervous system.

Additionally, a study in 2015 demonstrated that the antidepressant effects of ketamine are based on the release of BDNF and the activation of the L-type voltage-dependent calcium channels (VDCC). Researchers found that the release of BDNF regulates the antidepressant effects of ketamine, further clarifying the underlying mechanisms that ketamine utilizes.

Furthermore, researchers observed in another 2015 study that dysfunctional levels of BDNF may be linked to depression, and that ketamine treatment can produce a positive effect within certain pathways of the brain, such as in the prefrontal cortex and nucleus accumbens. In this animal study, rats were divided into four groups: saline+deprived, saline+non-deprived, ketamine+deprived, and ketamine+non-deprived. Ketamine infusions were administered daily for 14 days. Researchers then observed the animals’ brain structures. They observed that the deprived rats had reduced levels of BDNF in the amygdala, hippocampus and nucleus accumbens. The ketamine reversed the levels of BDNF in the amygdala and nucleus accumbens. This is important because the amygdala plays a critical response in fear and strong emotions, while the nucleus accumbens is essential in motivation, aversion, reward, and learning.

In addition to ketamine’s effect on the default mode network, neurons, brain waves, glutamate neurotransmitter, and inflammation, by understanding ketamine’s impact on BDNF, we can gain a deeper insight into the mystery of how our brain works. Ultimately, as Socrates once said, “To know thyself is the beginning of wisdom.”

References:

Choi, Miyeon, et al. “Ketamine Induces Brain-Derived Neurotrophic Factor Expression via Phosphorylation of Histone Deacetylase 5 in Rats.” Biochemical and Biophysical Research Communications, vol. 489, no. 4, 2017, pp. 420–425., doi:10.1016/j.bbrc.2017.05.157.

Lepack, A. E., et al. “BDNF Release Is Required for the Behavioral Actions of Ketamine.” International Journal of Neuropsychopharmacology, vol. 18, no. 1, 2014, doi:10.1093/ijnp/pyu033.

Réus, Gislaine, et al. “Ketamine Treatment Partly Reverses Alterations in Brain Derived- Neurotrophic Factor, Oxidative Stress and Energy Metabolism Parameters Induced by an Animal Model of Depression.” Current Neurovascular Research, vol. 12, no. 1, 2015, pp. 73–84., doi:10.2174/1567202612666150122122924.

Who should not get Ketamine?

Here are the 7 types of people who should NOT take ketamine:

  1. People with uncontrolled high blood pressure (hypertension). Ketamine is known to increase blood pressure, and in the setting of already high blood pressure the increase could get so high as to cause a heart attack or stroke. So it is important to have blood pressure monitored throughout your infusion.
  2. People with unstable heart disease (such as arrhythmias, congestive heart failure, coronary artery disease, etc.). Ketamine can increase heart rate and cardiac output (how hard your heart is working), which could worsen various heart conditions.
  3. People with untreated or uncontrolled thyroid disease (especially hyperthyroidism). In thyroid diseases such as hyperthyroidism, the body may already have an increased heart rate i.e. sympathetic overdrive which could be worsened with taking ketamine.
  4. People with active substance abuse. Ketamine can be used to treat addiction, however, infusions are given once the patient has detoxed or is off of the drugs the individual is addicted to. When a person is taking multiple drugs, the way their body may react may be unpredictable and potentially life threatening.
  5. People in an active manic phase of bipolar disorder. Ketamine can cause an altered mental state. If a person is already in an active manic state, ketamine could potentially worsen or enhance a worrisome emotional state.
  6. People with active delusions and hallucination symptoms (not taking prescription or while on street drugs). Similar to the point made in #5, a person can experience out of body experience or similar non ordinary state experiences when given ketamine. Ketamine could potentially enhance or worsen delusions and active hallucinations.
  7. Lastly, patients who have tried ketamine in the past and have had bad reactions to this medication.  If someone has been given ketamine for a procedure and had an adverse effect, we would suggest holding off. 

Psychedelic therapy, or at least the talk of them, is very popular as of this writing. Ketamine is currently the only legal and FDA approved psychedelic in the United States.  You may have heard about ketamine as a recreational drug or as an animal tranquilizer but not sure what to think about it. You may have depression, anxiety, OCD, or PTSD which is not being helped by standard treatments. You may even know of a loved one who could benefit from ketamine infusions. 

There is a lot of information out there. Some good and some not so good information in giving you a straight-forward understanding of ketamine as a treatment option for various mental health disorders. So welcome to our beginner’s guide, where we’ll cover the basics of what you need to know.

WHAT IS KETAMINE?

Ketamine was first synthesized in the 1960’s for use as a general anesthetic and FDA approved in 1970. Ketamine blocks the activity of glutamate (an excitatory neurotransmitter), which binds to and activates the NMDA receptor.  This NMDA receptor blockade is known to increase brain derived neurotrophic factor (BDNF).

Increases in BDNF results in increased neurogenesis and neuroplasticity. This helps those with chronic pain and depression to restore their neuronal activity and synaptic strength in the prefrontal cortex, restoring and resetting their brain back to a healthier state.

If you want to further learn how ketamine works check out: The 4 Mechanisms of How Ketamine Works

Ketamine has been traditionally used in the operating room and emergency departments for sedation and pain control.   Ketamine has a colorful history and is known to be used in veterinary medicine as a “animal tranquilizer” and even a recreational club drug of abuse.  However, ketamine is the most commonly medicine used worldwide for sedation and the World Health Organization (WHO) places ketamine in its List of Essential Medicines. 

Ketamine can be delivered into the body in several forms: oral (pill form), intranasal (insufflated into the nose), intramuscular (injected into the muscle), and intravenous (into the vein). Most ketamine clinics provide ketamine in the intravenous form as a slow infusion.  There are other clinics that may provide ketamine in the other forms in conjunction with psychotherapy. 

 WHY DOCTORS ARE USING KETAMINE?

Ketamine is effective in chronic pain, PTSD, depression, and other illnesses. Because of ketamine’s unique properties, many people are experiencing rapid, effective relief compared to traditional treatments, such as selective serotonin reuptake inhibitors (SSRIs) which can take months to take effect. 

When individuals are receiving ketamine for these treatments, ketamine is being used “off-label,” meaning that it is not being for the specific indication approved by the United States Food and Drug Administration (FDA). To get FDA approval for an indication, it requires multiple stages of research to evaluate the safety and efficacy for that specific use.  In 1970, ketamine was FDA approved for use as the,“sole anesthetic agent for diagnostic and surgical procedures that do not require skeletal muscle relaxation.”  But all other uses are considered “off-label.” Fortunately, once a drug is FDA approved, physicians have the freedom to use their best clinical judgment in prescribing drugs for other purposes than originally intended.  

WHO SHOULDN’T GET KETAMINE?

To understand who should not get ketamine, you’ll need to understand the effect of ketamine on the body. Ketamine can increase the heart rate and blood pressure, and stress the cardiac function of anyone who has uncontrolled heart problems.  Ketamine is used during medical procedures and operations for analgesia (i.e. doctors can perform surgeries and procedures without causing pain to the patients) due to its dissociative property. This dissociative property is also, according to research, associated with better antidepressant effect during ketamine infusions. While this is a wonderful property, if a person has a mental disorder which is characterized by hallucinations or delusions, undergoing ketamine infusions could actually worsen these conditions. 

REVISITING THE HALLUCINOGENIC POTENTIAL OF KETAMINE

WE NOW KNOW WHY KETAMINE IS SO EFFECTIVE AT TREATING DEPRESSION

FIRST KETAMINE INFUSION CLINIC IN PALM SPRINGS, CA OPENS

FROM CHAOS TO CALM: A LIFE CHANGED BY KETAMINE

IS KETAMINE THE NEXT BIG DEPRESSION DRUG?

KETAMINE RELIEVES DEPRESSION BY RESTORING BRAIN CONNECTIONS

IS KETAMINE THE BEST HOPE FOR CURING MAJOR DEPRESSION?

KETAMINE DEPRESSION TREATMENT ‘SHOULD BE ROLLED OUT’

KETAMINE: THE FUTURE OF DEPRESSION TREATMENT?

ONCE IT FULLY CATCHES ON, KETAMINE COULD BE A REALLY IMPORTANT ANTIDEPRESSANT

TACKLING DEPRESSION WITH KETAMINE

ONETIME PARTY DRUG HAILED AS MIRACLE FOR TREATING SEVERE DEPRESSION

YALE SCIENTISTS EXPLAIN HOW KETAMINE VANQUISHES DEPRESSION WITHIN HOURS

WHAT IT’S LIKE TO HAVE YOUR SEVERE DEPRESSION TREATED WITH A HALLUCINOGENIC DRUG

KETAMINE INFUSIONS CUT MIGRAINE PAIN IN HALF IN NEW STUDY

FOR RECALCITRANT NEUROPATHIC PAIN, CONSIDER OUTPATIENT KETAMINE

KETAMINE RESETS SYSTEM FOR NORMAL PAIN PROCESSING IN COMPLEX SYNDROME PATIENTS

FIBROMYALGIA DOCTOR TOUTS KETAMINE FOR PAIN AND DEPRESSION

FIBROMYALGIA PATIENTS TREATED WITH INTRAVENOUS KETAMINE

THIS COULD BE BIG: INTRAVENOUS KETAMINE FOR FIBROMYALGIA

THE CURRENT MENTAL HEALTH CRISIS AND THE COMING KETAMINE REVOLUTION

YALE: ‘MAGIC’ ANTIDEPRESSANT MAY HOLD PROMISE FOR PTSD

IV KETAMINE RAPIDLY EFFECTIVE IN PTSD

KETAMINE MAY HELP EXTINGUISH FEARFUL MEMORIES

KETAMINE COULD PROVE USEFUL IN TREATMENT OF SEVERE SOCIAL ANXIETY

PSYCHEDELIC MEDICINE 101: THE CURIOUS CASE OF KETAMINE

Links to Academic Articles

RAPID AND LONGER-TERM ANTIDEPRESSANT EFFECTS OF REPEATED KETAMINE INFUSIONS IN TREATMENT-RESISTANT MAJOR DEPRESSION

SAFETY AND EFFICACY OF REPEATED-DOSE INTRAVENOUS KETAMINE FOR TREATMENT-RESISTANT DEPRESSION

NEUROBIOLOGY OF STRESS, DEPRESSION, AND RAPID ACTING ANTIDEPRESSANTS: REMODELING SYNAPTIC CONNECTIONS

NEW PARADIGMS FOR TREATMENT-RESISTANT DEPRESSION

ANTIDEPRESSANT EFFICACY OF KETAMINE IN TREATMENT-RESISTANT MAJOR DEPRESSION: A TWO-SITE RANDOMIZED CONTROLLED TRIAL

HIPPOCAMPAL VOLUME AND THE RAPID ANTIDEPRESSANT EFFECT OF KETAMINE

KETAMINE AND THE NEXT GENERATION OF ANTIDEPRESSANTS WITH A RAPID ONSET OF ACTION

DO THE DISSOCIATIVE SIDE EFFECTS OF KETAMINE MEDIATE ITS ANTIDEPRESSANT EFFECTS?

SYMPTOMATOLOGY AND PREDICTORS OF ANTIDEPRESSANT EFFICACY IN EXTENDED RESPONDERS TO A SINGLE KETAMINE INFUSION.

ANTIDEPRESSANT EFFECTS OF KETAMINE IN DEPRESSED PATIENTS

THE ROLE OF KETAMINE IN TREATMENT-RESISTANT DEPRESSION: A SYSTEMATIC REVIEW

IMPROVEMENT IN SUICIDAL IDEATION AFTER KETAMINE INFUSION: RELATIONSHIP TO REDUCTIONS IN DEPRESSION AND ANXIETY

USE OF KETAMINE IN ACUTE CASES OF SUICIDALITY

A POSSIBLE ROLE FOR KETAMINE IN SUICIDE PREVENTION IN EMERGENCY AND MAINSTREAM PSYCHIATRY

EFFICACY OF INTRAVENOUS KETAMINE FOR TREATMENT OF CHRONIC POST-TRAUMATIC STRESS DISORDER: A RANDOMIZED CLINICAL TRIAL

EFFICACY OF KETAMINE IN THE TREATMENT OF SUBSTANCE USE DISORDERS: A SYSTEMATIC REVIEW

KETAMINE REDUCES MUSCLE PAIN, TEMPORAL SUMMATION, AND REFERRED PAIN IN FIBROMYALGIA PATIENTS

KETAMINE IN CHRONIC PAIN MANAGEMENT: AN EVIDENCE-BASED REVIEW

RANDOMIZED CONTROLLED CROSSOVER TRIAL OF KETAMINE IN OBSESSIVE-COMPULSIVE DISORDER: PROOF-OF-CONCEPT

RAPID RESOLUTION OF OBSESSIONS AFTER AN INFUSION OF INTRAVENOUS KETAMINE IN A PATIENT WITH TREATMENT-RESISTANT OBSESSIVE-COMPULSIVE DISORDER: A CASE REPORT

ANALGESIC EFFECT OF SUBANESTHETIC INTRAVENOUS KETAMINE IN REFRACTORY NEUROPATHIC PAIN: A CASE REPORT

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SingleCare Guide to medication Management

 SingleCare just published a piece called Seniors’ Guide to Medication Management, which covers important tips and tricks for seniors and their caregivers to properly handle prescriptions.

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It’s not uncommon for seniors to be placed on an extensive medication regimen. We created this guide to educate people on how to safely simplify this often complicated process. The guide offers practical advice on:

  • How to accurately read medication labels
  • Ways that aging changes your responses to medications
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Depression Ketogenic Diet

Ketamine Therapy Center in Fairfax, VA | 703-844-0184 | Ketamines for Depression | Ketogenic Diets for Mood stabilization

Can a Ketogenic Diet Benefit Patients With Mental Health Disorders?

For more than 50 years, researchers have examined the effect of a ketogenic diet on patients with behavioral health disorders.1 Despite this breadth of research, most of the studies have lacked depth, consisting mostly of case reports, animal studies, and small-sample open studies rather than controlled trials.1 Although researchers remain cautious, a review of research reveals that the popular diet may hold some promise for individuals with mental health disorders.

How Does the Ketogenic Diet Affect the Brain?

The ketogenic diet is an established option for treatment-resistant epilepsy, as evidenced by a range of studies, including controlled trials.1 The diet also has shown promise for managing other brain-based disorders, such as Parkinson disease, amyotrophic lateral sclerosis, traumatic brain injury, multiple sclerosis, and chronic headaches as well as for metabolic disorders such as obesity, cancer, and type 2 diabetes.2

Unfortunately, it is unclear how ketogenic diets work to control seizures, let alone how they may improve psychiatric symptoms.2 It may pertain to the presence of ketones, reduction in blood sugar, reduction in insulin and other growth-promoting hormones, or the combination of all of these.2 Other theories include altered neurotransmitter levels, changes in electrolyte gradients (lower intracellular sodium and calcium), reduction in markers of inflammation, and improved mitochondrial function.2

“The general consensus is that the brain functions more cleanly and efficiently when a significant portion of its energy comes from ketones, calming overactive and overly reactive brain cells,” Georgia Ede, MD, a board-certified psychiatrist specializing in nutrition-focused counseling, explained in Psychology Today.2

What the Research Reveals

A review of the literature reveals the following about the ketogenic diet’s reaction with diseases1:

  • Anxiety: Exogenous ketone supplementation reduced anxiety-related behaviors in a rat model.
  • Attention-deficit/hyperactivity disorder: In a controlled trial of the ketogenic diet in dogs with comorbid epilepsy, both conditions significantly improved.
  • Autism-spectrum disorder: An open-label study in children reported no significant improvement, yet one case study reported “a pronounced and sustained response.” Further, in 4 controlled animal studies, the ketogenic diet significantly reduced autism-related behaviors in mice and rats.
  • Bipolar disorder: One case study reported a reduction in symptomatology whereas a second case study reported no improvement.
  • Depression: The ketogenic diet significantly reduced depression-like behaviors in rat and mice models in 2 controlled studies.
  • Schizophrenia: An open-label study in female patients found reduced symptoms after 2 weeks of the ketogenic diet whereas a single case study reported no improvement; however, 3 weeks of the ketogenic diet in a mouse study normalized pathological behaviors.

The Bostock review did not include studies regarding how the ketogenic diet affects dementia and Alzheimer disease. A 6-week study of a low-carbohydrate diet in persons with mild cognitive impairment saw improvement in verbal memory, with greater benefits for persons who achieved higher ketone levels.2 The cognition and function of a man with Alzheimer disease “significantly improved” with the use of ketone supplements during a 20-month case study.2

A review of the effect of the ketogenic diet on patients with epilepsy concluded that3:

  • Subjective assessment of patients found cognitive improvements with the ketogenic diet treatment, particularly in the domains of alertness, attention, and global cognition;
  • Studies that used objective neuropsychological tests, however, confirmed benefits in alertness but found no improvement in global cognition;
  • The duration of the ketogenic diet treatment appears to have a positive effect on the degree of cognitive improvement; and
  • Because patient compliance with the ketogenic diet is generally low, this may lead to a bias in the research.

Researchers Urge Caution

According to researchers, there are several reasons why the effectiveness of the ketogenic diet in mental disorders is difficult to prove1:

  • Low number of human studies
  • Low quality of the studies (sample sizes are small, no control for placebo effects, no consistent measurement of ketosis, lack of detail about the specifics of the diet and duration)
  • No enforced standards as to what constitutes the ketogenic diet in humans
  • Ketogenic diet monotherapy is largely unexamined in human studies
  • The ketogenic diet requires patients who may be ill to measure food portions
  • Diet compliance can be difficult, particularly for patients with mania, apathy, reduced appetite, food cravings, or binge eating issues

The ketogenic diet may also cause adverse effects, including1,2:

  • Constipation
  • Elevated liver enzymes and/or abnormal liver function
  • Elevated serum cholesterol
  • Elevated triglycerides
  • Emesis
  • Gallstones
  • Hemolytic anemia
  • Hypoglycemia
  • Hypoproteinemia
  • Kidney stones
  • Leg cramps
  • Menstrual irregularities
  • Periorbital edema
  • Presacral edema
  • Renal tubular acidosis
  • Thrombocytopenia
  • Unwanted weight loss
  • Viral gastroenteritis

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Dr Ede agreed that the research is not there — yet.

“Nutrition studies are hard. Blinding is nearly impossible, funding is hard to come by, compliance is challenging, and controls are difficult to design,” Dr Ede explained.2 “Fear, bias, and nutrition miseducation limit the number of scientists interested in and willing to conduct studies of low-carbohydrate, high-fat diets. We clearly need high-quality human studies exploring the effects of ketogenic diets on mental health disorders, as many clinicians and patients will be afraid to utilize this diet without stronger evidence.”2

Most researchers agree that low-carbohydrate diets can help stabilize brain chemistry, particularly for patients who are not responding to other treatments. Psychiatrists interested in recommending the ketogenic diet to a patient may benefit from consulting with a dietitian or primary care provider with expertise in ketogenic diets.2

References

  1. Bostock EC, Kirkby KC, Taylor BV. The current status of the ketogenic diet in psychiatryFront Psychiatry. 2017;8:43.
  2. Ede, G. (2017). Ketogenic diets for psychiatric disorders: a new 2017 reviewPsychology Today. [Accessed 9 Aug. 2019].
  3. van Berkel AA, Ijff DM, Verkuyl JM. Cognitive benefits of the ketogenic diet in patients with epilepsy: a systematic overviewEpilepsy Behav. 2018;87:69-77. 

Ketogenic Diets for Psychiatric Disorders: A New Review

Ketogenic Diets Yesterday, Today and Tomorrow

Freepik

Source: Freepik

If you have a brain, you need to know about ketogenic diets. The fact that these specially-formulated low-carbohydrate diets have the power to stop seizures in their tracks is concrete evidence that food has a tremendous impact on brain chemistry and should inspire curiosity about how they work. I first became interested in ketogenic diets as a potential treatment for bipolar mood disorders, given the many similarities between epilepsy and bipolar disorder

Ketogenic diets have been around for about 100 years, and have proved to be invaluable tools in the treatment of stubborn neurological conditions, most notably epilepsy. They have also shown promise in the management of other brain-based disorders such as Parkinson’s Disease, ALS, Traumatic Brain Injury, Multiple Sclerosis, and chronic headaches, as well as in metabolic disorders like obesity, cancer, and type 2 diabetes.

But where does the science currently stand on the ketogenic diet and psychiatric disorders like bipolar disorderschizophrenia, and Alzheimer’s Disease? How many human studies do we have, and what do they tell us? If you are struggling with mood, attention, or memory problems, should you try a ketogenic diet? If you are a clinician, should you recommend a ketogenic diet to your patients?

A recent review article The Current Status of the Ketogenic Diet in Psychiatry by researchers at the University of Tasmania in Australia [Bostock et al 2017 Front Psychiatry 20(8)] brings us nicely up to date on all things ketogenic and mental health. I summarize the paper below and offer some thoughts and suggestions of my own. [Full disclosure: I am a psychiatrist who studies nutrition and eats a ketogenic diet.]

First, some basics for those of you who are unfamiliar with these special diets.

What are Ketogenic Diets?

Definitions vary, but what all ketogenic diets have in common is that they are very low in carbohydrate (typically 20 grams per day or less) and relatively high in fat. The goal is to lower blood sugar and insulin levels; when these are nice and low, the body naturally turns to fat (instead of sugar) as its primary source of energy. Most ketogenic diets also limit protein (to no more than the body requires), because excess protein can raise blood sugar and insulin levels to some extent. Body fat and fat from the diet then break down into ketones, which travel through the bloodstream and can be burned by various cells throughout the body, including most brain cells. Ketone levels rise in the blood, urine and breath within days, and can be measured using various home test methods, but it can take weeks for the body to become efficient at burning fat for energy, and for full benefits to be realized.

When a person is “in ketosis”, fasting morning blood glucose levels tend to average between 60 and 85 (mg/dl), and blood ketone levels rise to at least 0.5 mM (with much higher levels recommended for certain conditions). These parameters distinguish ketogenic diets from other low-carbohydrate diets, which may contain too much protein and/or carbohydrate to produce these metabolic effects.

How do Ketogenic Diets Work?

It remains unclear how ketogenic diets work to control seizures, let alone how they may improve psychiatric symptoms. On a fundamental level, we are not even sure whether it is the presence of ketones, the reduction in blood sugar, the reduction in insulin and other growth-promoting hormones, or the combination of all of these which are responsible for the brain-stabilizing effects of these diets. Theories abound, and include altered neurotransmitter levels, changes in electrolyte gradients (lower intracellular sodium and calcium), reduction in markers of inflammation, and improved mitochondrial function. The general consensus is that the brain functions more cleanly and efficiently when a significant portion of its energy comes from ketones, calming overactive and overly-reactive brain cells.

What about Ketone Supplements?

You can raise your blood ketone levels without changing your diet, by either taking expensive ketone supplements or by ingesting fats high in medium chain triglycerides (MCTs), which the liver rapidly transforms into ketones. Purified MCTs are available for purchase, or you can simply take coconut oil, which is naturally rich in MCTs. You’ll see below that these approaches can be effective short-term, but my opinion is that they simply mask the underlying disease, which continues to worsen due to ongoing high insulin and/or blood glucose levels.

SUMMARY OF THE SCIENCE

I’ve listed all relevant studies covered in the 2017 Bostock review below, paying special attention to the human studies, and supplementing with original source material where helpful, as there were some minor errors in the text of the review. 

Ketogenic Diets and Bipolar Disorder

2002: A one-month case study of a woman with unspecified, treatment-resistant bipolar disorder noted no improvement after two weeks on a ketogenic diet followed by two weeks of MCT oil supplementation. Urine testing found ketosis was never achieved.

2012: A case study of two women with bipolar II disorder who ate a ketogenic diet (one for two years, the other for three years) found that the diet was superior to the anticonvulsant/mood stabilizer lamotrigine (Lamictal) in management of symptoms. Ketosis was documented using urine test strips.

Ketogenic Diets and Schizophrenia

A 3-week mouse study showed that a ketogenic diet normalized pathological behaviors.

1965: A 2-week study of 10 women with treatment-refractory schizophrenia found a significant decrease in symptoms when a ketogenic diet was added to their ongoing standard treatments (medications + ECT). Ketone monitoring was not reported.

2009: A 12-month case study details the experience of a 70-year old overweight woman with chronic schizophrenia who was prescribed a diet limited to 20 grams of carbohydrate per day. She noted significant improvement in severe symptoms beginning only eight days after starting the diet, which consisted of “beef, poultry, ham, fish, green beans, tomatoes, diet drinks, and water.” [ Kraft and Westman 2009 Nutrition & Metabolism 6:10.] She reported complete resolution of auditory and visual hallucinations–with which she’d suffered since age seven. Ketone levels were not monitored.

Comment: This diet is best characterized as a low-carbohydrate, primarily whole foods diet. As protein wasn’t limited and fat intake wasn’t manipulated, this may or may not have been a truly ketogenic diet.

Ketogenic Diets and Anxiety

A rat study found that adding ketone supplements to a standard high-carbohydrate diet reduced anxious behavior.

Ketogenic Diets and Depression

A rat study found that a ketogenic diet reduced depressive behaviors.

A mouse study found that feeding pregnant animals a ketogenic diet reduced offspring susceptibility to depressed (and anxious) behaviors.

Ketogenic Diets and Autism Spectrum Disorder (ASD)

A 70-day mouse study found that a ketogenic diet improved behavior.

A 10-14 day rat study found that a ketogenic diet improved complex social behaviors and mitochondrial function.

A 3-4 week mouse study found that a ketogenic diet improved behaviors in ways that were different for males than females.

2003: A 6-month inpatient study evaluated the effects of a cyclical ketogenic diet (4 wks on, 2 wks off) on 30 children with ASD. Of the 18 children who completed the study, eight showed moderate improvement, and two showed “significant” improvement. Benefits appeared to persist even during the 2-week “diet-free” periods. Urine and blood ketone monitoring confirmed that all children were in ketosis.

Comment: blood ketone levels ranged from 1.8 to 2.2 mMol during ketogenic phases and from 0.8 to 1.5 mMol during “diet-free” periods, meaning that the children actually spent the entire 6-month study period in ketosis.

2013: A 14-month detailed case study of one child with ASD, epilepsy, and obesity who was placed on a ketogenic diet in combination with anti-epileptic medications, noted numerous improvements. “In addition to improvement in seizures, there was a 60-pound weight loss…as well as improved cognitive and language function, marked improvement in social skills, increased calmness, and complete resolution of stereotypies.” [Herbert and Buckley 2013 J Child Neurol 28(8)]. Ketosis was confirmed (presumably by urine testing).

Ketogenic Diets and ADHD (Attention Deficit Hyperactivity Disorder)

A 6-month study of dogs with ADHD and epilepsy found significant improvement in ADHD behaviors on a ketogenic diet.

Ketogenic Diets and Alzheimer’s disease

2009: A 90-day randomized, double-blind, placebo-controlled, parallel study of 152 people with mild to moderate Alzheimer’s Disease tested the effects of a daily MCT supplement (previously marketed under the name Axona) on cognitive test performance. People continued their usual diets and took either the MCT supplement or a safflower oil placebo. Regular medications were continued throughout the study. At 45 and 90 days, patients taking MCTs showed significant improvement on a cognitive test known as the ADAS-Cog scale, unless they carried a gene called ApoE4, which is associated with higher risk for Alzheimer’s disease. Cognitive benefits did not persist after MCTs were discontinued.

Not mentioned in the Bostock review are the following two studies:

 1) A 6-week study of a simple low-carbohydrate diet (protein and fat unrestricted) in people with mild cognitive impairment (MCI, aka “pre-Alzheimer’s” disease) demonstrating improvement in verbal memory, with greater benefits seen in those who achieved higher ketone levels [Krikorian R et al 2012 Neurobiol Aging 33(2):425].

 2) A 20-month case study of a man with Alzheimer’s Disease whose cognition and function significantly improved with the use of ketone supplements [Newport MT et al 2015 Alzheimer’s & Dementia 11] .

Please also see my Psychology Today article Preventing Alzheimer’s Is Easier Than You Think.

Limitations of the Research

If you are a ketogenic diet skeptic, you will find the above summary unimpressive. I can’t blame you—there is precious little human data about ketogenic diets and psychiatric disorders, and what is there is flawed: small sample sizes, no controls, ketosis unconfirmed in some cases, diet composition and length of treatment variable between studies, etc. However, as a low-carbohydrate diet enthusiast, I find much to be excited about in this ragtag fugitive fleet of papers.  

Nutrition studies are hard. Blinding is nearly impossible, funding is hard to come by, compliance is challenging, and controls are difficult to design. Fearbias, and nutrition miseducation limit the number of scientists interested in and willing to conduct studies of low-carbohydrate, high-fat diets. We clearly need high-quality human studies exploring the effects of ketogenic diets on mental health disorders, as many clinicians and patients will be afraid to utilize this diet without stronger evidence. If only more people held the USDA Dietary Guidelines to the same scientific standard and eyed it with the same healthy skepticism…

Ketogenic Diets in the Real World

Nevertheless, I believe in the therapeutic potential of low-carbohydrate diets to stabilize brain chemistry, and feel strongly that people should be made aware of dietary strategies as an option. For people who don’t want to take medication, haven’t responded to medication, can’t tolerate medication or can’t afford medication, nutritional intervention can offer real hope and empowerment. I personally noticed an overall improvement in concentration, mood, energy, and productivity when I changed my own diet years ago, and have witnessed people in my own practice whose mood stabilized by switching to a low-carbohydrate, high-fat, whole foods diet. My philosophy regarding the dietary treatment of mental health problems is as follows:

  1. Everyone should eat real, whole foods and minimize refined carbohydrates like sugar and flour. Most view this as common sense advice (with the notable exception of the USDA). I personally recommend a pre-agricultural dietary pattern (which includes animal protein/fat and eliminates grains/legumes). 
  2. Those with insulin resistance (including those with type 2 diabetes) would be wise to make lifestyle changes that can help to normalize insulin and blood sugar levels. Strategies with the potential to accomplish this include simple low-carbohydrate diets, intermittent fasting, strength training, and caloric restriction. Education, professional guidance, support and medical monitoring are important to have in place before trying dietary changes, particularly if you have any health problems or take any medications. 
  3. Individuals who have not benefited from the above changes or who simply want to try a different approach may wish to consider a ketogenic diet.

It could be many years before we see high-quality studies of ketogenic diets in the treatment of psychiatric disorders. For those of you who don’t want to wait that long—what do you need to know?

Ketogenic Diet Safety and Side Effects

The ketogenic diet is safe for most people, but there are clear exceptions to consider that go beyond the scope of this post, so please do not embark on a ketogenic diet yourself nor recommend it to someone else without first reading my detailed article Ketogenic Diets and Psychiatric Medications, my short post Is the Ketogenic Diet Safe for Everyone? and seeking additional guidance and resources to educate yourself about the diet. Two of the best books on the subject are The Art and Science of Low Carbohydrate Living by Drs. Phinney and Volek, and The New Atkins for a New You by Dr. Eric Westman.

Some studies report side effects such as constipation, leg cramps, and increased risk of kidney stones. There are very real shifts in salt and fluid balance that occur in the early stages of the diet that may explain some of these side effects, but most people tolerate the diet well, including myself. My opinion is that the majority of side effects are not due to the low-carbohydrate, high-fat nature of the diet, but rather due to food choices. Unfortunately, most ketogenic diets, particularly those prescribed to children with epilepsy, are high in processed/artificial ingredients, and foods that many people are sensitive to, such as nuts, dairy, eggs, and biogenic amines.

If you are a psychiatric clinician interested in recommending the ketogenic diet to a patient, I highly recommend collaborating with a dietitian, primary care provider, or specialist with expertise in ketogenic diets. If there isn’t such an individual in your area, there are other options, including specialty dietitians and medical centers offering on-line consultation. 

2003: A 6-month inpatient study evaluated the effects of a cyclical ketogenic diet (4 wks on, 2 wks off) on 30 children with ASD. Of the 18 children who completed the study, eight showed moderate improvement, and two showed “significant” improvement. Benefits appeared to persist even during the 2-week “diet-free” periods. Urine and blood ketone monitoring confirmed that all children were in ketosis.

The Carnivore Diet for Mental Health?

How plant-free diets affect the brain

arnivore Curious?

Last month, I had the pleasure of participating in the Boulder Carnivore Conference, the world’s first meeting dedicated to the potential benefits of plant-free diets. For this special event, I created a new presentation exploring the nutritional differences between plant and animal foods, and summarizing the scientific arguments in support of all-meat diets for optimal brain health. Skeptical? You should be. This seemingly strange and extreme way of eating flies in the face of every piece of conventional nutrition advice we’ve been given, yet a growing number of people report  remarkable benefits, including resolution of serious, chronic psychiatricsymptoms. If you are curious about how this diet might help to correct chemical imbalances in the brain, please watch this video to learn more.

If you are completely new to the idea of all-meat diets, allow me to provide a bit of context, along with some additional links and resources should you care to dive a little deeper.

*An update in response to concerns expressed in the comments section: No, I am not funded by the meat industry. My nutrition work is >95% self-funded. I have no financial conflicts of interest that might bias me towards animal foods. I do acknowledge intellectual bias towards animal foods, as I’m convinced by the science (see video and resource following this article), my clinical experience, and my own personal experience (see below) that they are important to human health.

Interest in Plant-free Diets Takes Root

Have you heard? The so-called “carnivore” diet—a diet completely free of plant foods—has become something of a hot new micro-trend, thanks in part to several high-profile adopters who report that switching to an all-meat diet significantly improved their mental and physical health.

One of these ambassadors of carnivory is Mikhaila Peterson, a 27-year old Canadian woman who credits a meat-only diet not only for putting her juvenile rheumatoid arthritis into remission (no small feat, as JRA, is a serious and destructive autoimmune disease), but also for her complete recovery from the severe depression and anxiety she’d suffered with since the fifth grade.

Mikhaila first became aware of the carnivore diet after hearing Dr. Shawn Baker talk about the benefits of his all-beef diet on the Joe Rogan Experience podcast. Dr. Baker is a California-based orthopedic surgeon and multi-sport elite athlete who actively promotes the carnivore diet on social media and explores its theory and practice on his popular Human Performance Outliers podcast

Mikhaila’s experience inspired her father, well-known University of Toronto psychologist Professor Jordan Peterson, to try the diet in an attempt to alleviate his own depression. He has since reported alleviation of not only depression and anxiety but also of a number of bodily ailments including psoriasis and gastric reflux, as detailed in this article in The Atlantic. 

The Boulder Carnivore Conference was the brainchild of Colorado-based Amber O’Hearn, a data scientist, nutrition science writer and public speaker who has adhered to a carnivore diet since 2009. She produces thoughtful, meticulously-researched articles about the science of animal-based nutrition on her website Empirica and is writing a book dedicated to this topic. In interviews such as this one, she explains how her unusual way of eating seemed to resolve her symptoms of bipolar depression, including suicidalideation, which psychiatric medications had failed to accomplish.

Carnivore Diets and Psychiatric Disorders

As a psychiatrist specializing in nutrition, I work with people to help troubleshoot, customize and optimize their diets to improve their mental health, with the goal of reducing or in some cases even eliminating the need for psychiatric medications. There are many different dietary strategies that can help people achieve this goal—removing processed foods, carefully supplementing whole food plant-based diets, ketogenic diets, etc. It’s important to emphasize that most people probably don’t need to go to the extreme of removing all plants from their diet in order to experience relief, and of course, no diet, including a carnivore diet, will work for everyone. 

All that being said, I have consulted with many people who report significant mental health benefits on low-plant and plant-free diets. While I am not at liberty to share the details of these confidential cases, numerous compelling, public first-hand personal accounts of psychiatric conditions resolving on all-meat diets exist, including this interview with 58-year-old West Virginia-born musician Brett Lloyd and this conversation with Andrew Graf, a young entomologist in Texas, both conducted by Boston-based host Scott Myslinski on his CarnivoreCast podcast. Dr. Baker curates a wonderful collection of mental health testimonials at meatheals.com, which contains 110 entries to date.

I count myself among the believers [I use the word “believers” intentionally to underscore the fact that clinical trials of the carnivore diet do not yet exist.]  In 2008 I reversed symptoms of fibromyalgia, chronic fatigue, migraines, and IBS by gradually removing most plant food from my diet. As a psychiatrist, I was fascinated to observe that my mood, energy, sleep, and concentration improved significantly as well. I share more about my story in this video interview with Ivor Cummins.  [I switched from a very low-plant ketogenic diet to a pure carnivore diet in June 2018, long after this conversation took place]. It was that extraordinary experience that called me to question conventional beliefs about food and health, gave birth to my passion for the study of nutrition science, and led eventually to my first public presentation in 2012 Little Shop of Horrors: the Risks and Benefits of Eating Plants.

As surprising and powerful as these stories are, they are just anecdotes…they do not constitute formal scientific evidence. Perhaps all of these alleged improvements could be chalked up to exaggeration, wishful thinking, or coincidence. It is up to you whether you choose to dismiss them, become genuinely curious about them, or feel inspired by them. I lay out the scientific arguments supporting this way of eating in my video but clinical trials do not yet exist. 

If remarkable stories of chronic mental illness being put into remission through all-meat diets are to be believed, we have to ask why. Why might a diet completely devoid of the plant foods we are told to be so healthy for us be—at least in some cases— ostensibly healthier for the brain than one containing plants?

Look Before You Leap

If you are inspired to try a carnivore diet for mental health purposes, and you currently take psychiatric medications (or medications of any kind), please read my article Ketogenic Diets and Psychiatric Medications first. Just as with a standard low-carbohydrate or ketogenic diet, carnivore diets cause profound shifts in brain and body chemistry rather quickly. These changes are almost always positive and healthy, but they can have a major impact on medication levels, dosages, and side effects that require close medical supervision, particularly in the first month or two while your metabolism adjusts to your new healthy way of eating. It is very important to consult with your prescribing clinician before embarking on any low-carbohydrate diet. article continues after advertisement

For More Information

If you prefer written arguments (fully referenced) to videos or would like to learn more about the arguments outlined in the video, you may find the following articles of interest:

Your Brain on Plants: Micronutrients and Mental Health

The Brain Needs Animal Fat

Do You Have Arachiphobia?

Which Diet Is Healthiest for the Brain?

The Antioxidant Myth

Low Brain Cholesterol—Separating Fact from Fiction

Do We Really Need to Eat Our Vegetables?

Ketogenic Diets for Psychiatric Disorders: A New 2017 Review

Little Shop of Horrors? The Risks and Benefits of Eating Plants

What is the Carnivore Diet? Potential Benefits and Concerns (by nutrition therapist Amy Berger)

The Ultimate Guide to the Carnivore Diet (by Raphael Sirtoli and Amber O’Hearn)

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