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

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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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