In the two preceding blog posts, we’ve reviewed the multiple causes of depression, and why anti-depressants are not effective in the treatment of mild to moderate symptoms. Now we’re going to review a wide variety of treatment approaches.
Fortunately, a number of relaxation techniques and coping styles can improve depression, further emphasizing the role of stress in depression. These approaches include Mindfulness-Based Stress Reduction, meditation, biofeedback, progressive muscle relaxation and an integrative health approach that combines relaxation, nutrition, and exercise/
Recent studies suggest some of these techniques influence genetic activity regulating depression. Brain imaging techniques show meditation significantly affects neurotransmitter levels and the activity of various parts of the brain that facilitate relaxation.
Preliminary research suggests that two nutrients, coenzyme Q10 and acetyl-L-carnitine, which support mitochondrial function, may influence depression. A small study of 35 depressed patients in comparison to 22 healthy volunteer controls showed that plasma CoQ10 levels were significantly lower in the depressed patients. Levels were also lower in treatment-resistant patients, as well as those with chronic fatigue.
Several studies of geriatric depression have investigated acetyl-L-carnitine. One study compared treatment with acetyl-L-carnitine to the medication amisulpride, an antipsychotic medication commonly used to treat depression. In 204 patients with chronic depression, both acetyl-L-carnitine and the pharmaceutical drug improved symptoms. Acetyl-L-carnitine also has been found to relieve depression and improve quality of life in patients with liver disease, and to ease depressive symptoms significantly in patients with fibromyalgia.
Another nutrient, pyrroloquinoline quinine (PQQ), is an enzyme involved in the generation of new mitochondria and the maintenance of antioxidant defense systems. Supplemental PQQ has been shown to increase mitochondrial activity levels and to be neuroprotective in animal models. Since fewer mitochondria have been observed in depressed patients, PQQ may be supportive in this population.
Cognitive Behavioral Therapy
Cognitive behavioral therapy (CBT) is a non-pharmacologic means of therapy often employed to relieve depression. CBT is typically initiated if primary treatment with antidepressant medications fail, but it is sometimes used as part of first-line treatment alongside antidepressants.
CBT is centered upon the belief that depression is closely linked with negative thinking (i.e. thought patterns that negatively reinforce depressed mood). The goal of CBT is to help the patient recognize and replace negative thinking with more positive, constructive thoughts. CBT has been studied in various settings and has shown efficacy both independently and in combination with other conventional treatment regimens.
A recent review of studies using CBT in treatment resistant depression found that CBT performed as well as pharmacotherapy when used in conjunction with a primary medication, or in cyclical fashion involving switching from pharmacotherapy to CBT and back again. This same review also pointed out that when a patient with treatment resistant depression switched antidepressants, greater relief was attained when the switch was accompanied by CBT. A 2010 clinical trial revealed that CBT effectively relieved depression and/or anxiety in patients with chronic obstructive pulmonary disease.
CBT is also effective in young people with depression, and may be preferable over psychotropic drugs for some parents since it lacks harsh side effects. In one trial, CBT was compared to stand-of-care (pharmacotherapy) in children ages 8 – 15. CBT was superior to pharmacotherapy in several aspects, including patient alliance to treatment. Moreover, CBT may have an overall cost advantage versus pharmacotherapy.
It is imperative if you have depression to talk with a qualified healthcare provider about cognitive behavioral therapy as an adjuvant, or alternative to pharmacotherapy.
Research supports the use of exercise, primarily aerobic or weight training, as a preventive and adjuvant treatment (used in conjunction with medication) of mood disorders and depression. Some studies have found exercise alone is as effective as medication for relieving depression and that exercise can reduce depression recurrence rates. A recent study involved 202 adults with major depression who either participated in 4 months of exercise, took the medication sertraline, or took a placebo. A one-year follow up showed that exercise was as effective as the medication at relieving depression and that exercise during the follow-up period extended the benefits.
Research shows morning light therapy from a light-therapy lamp is effective at treating seasonal affective disorder (seasonal depression), and that it is equally or possibly even more effective than antidepressants, in this type of depression. A study of 98 patients with seasonal depression illustrated this. Depressed subjects were randomly assigned to 8 weeks of therapy with light in the morning (30 minutes, 10,000 lux, and a placebo pill) or 30 minutes of dim light (100 lux and 20 mg of fluoxitine), with both groups experiencing a 67 % response rate.
While the results are promising, light therapy for non-seasonal depression is not well established and may be more helpful as a complementary therapy rather than as a stand-alone treatment.
Thyroid dysfunction may be a significantly underappreciated cause of depressive symptoms. In one study, thyroid disorders were associated with a 22% higher likelihood of depression in women.
Studies have shown that treating subjects within so-called “normal” thyroid hormone levels may still be beneficial. In one such pilot study invloving 17 female patients with depression, 11 (64.7%) saw significant improvement in response to a moderate dose of l-thyroxine (Lojko 2007). Similarly, in a study of 225 subjects with treatment resistant depression, augmenting primary antidepressant therapy with thyroid hormone was found to be roughly as effective as adding a second antidepressant medication for providing relief of symptoms.
DHEA is an important steroid hormone often referred to as a neurosteroid because it serves a variety of functions in the brain. DHEA levels decrease with age and stress, and people with depression often have low levels of DHEA. In one study, blood samples from women with a history of depression contained lower levels of select neurosteroids, including DHEA, than women with no depression history. Experiments found women with a history of depression may metabolize progesterone differently than healthy women, reflecting an adaptive effort by the body to compensate for low neurosteroid levels.
A number of studies have examined the role of DHEA in depression, with very encouraging results. DHEA has been shown to modulate serotonin levels in the brains of laboratory animals. DHEA has also performed well in human trials. DHEA therapy significantly benefited patients with HIV/AIDS and depression. In a randomized, placebo-controlled, double-blind study, researchers studied the effects of 90 mg DHEA daily for 3 weeks and 450 mg daily for 3 weeks as a stand-alone treatment for both mild and severe depression. They found that DHEA therapy resulted in a significant improvement in symptoms compared with the placebo.
Melatonin is a hormone produced in the pineal gland in the brain; it is involved in sleep-wake function and other circadian rhythms. Melatonin decreases with age and some studies link low levels of melatonin with symptoms of depression.
A double-blind placebo-controlled pilot study of perimenopausal and post-menopausal women who took 3 mg of melatonin at bedtime for 6 months showed significant improvement in depressive symptoms. Recently, another well-controlled preliminary study looked at 33 participants with major depression and early morning waking who took 6 mg of melatonin for 4 weeks. The results suggested improvement in sleep and depressive symptoms.
Studies of the medication agomelatine, which acts upon melatonin receptors in the brain, support melatonin’s influences on depression. Some studies suggest that this drug may be as effective as venlafaxine, fluoxetine, and sertraline in relieving depression.
Nutrients to Balance Brain Chemistry
Depression is a multifactorial condition, and efficient relief requires addressing multiple neurochemical and metabolic imbalances that may underlie mood disturbances. The nutrients listed in the protocol are categorized according to their evidence-based mechanisms of action in brain health and mood regulation. The categories are:
- Broad-range nervous system function (omega-3 fatty acids, magnesium);
- Neurotransmitter synthesis (SAMe, folate, B12 , B6, tryptophan, 5-HTP, );
- Blood-sugar regulation (chromium, green coffee extract);
- Antioxidant effects (lipoic acid, NAC, selenium); and
- Others (St. John’s Wort, vitamin D, zinc, inositol, iron).
Broad-Range Nervous System Effects: Omega-3 Fatty Acids and Magnesium
Omega-3 fatty acids
Omega-3 fatty acids are long-chain polyunsaturated fatty acids found in fish and various oils, such as flaxseed or coconut oil. The brain has a high concentration of polyunsaturated fatty acids, which are found mostly in cell membranes. They affect adaptability of the nervous system, nerve cell conduction and function, and neurotransmitter synthesis. Several research models exhibit the influence of omega-3 fatty acids in depression including: (a) dietary studies; (b) nutritional status studies showing positive effects associated with higher omega-3 to omega-6 fatty acid ratios; and (c) intervention studies that look at both eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) taken as a stand-alone treatment and as an adjunct to medication.
One investigation showed that adding the omega-3 fatty acid EPA to conventional antidepressant treatment relieved depressive symptoms. Among children with depression, supplementation with omega-3 fatty acids demonstrated “highly significant” effects on symptom scores. In a review article from 2006, researchers analyzed results from six published studies and found that omega-3 fatty acids can reduce symptoms of depression among adults as well.
Omega-3 fatty acids are counterbalanced with the inflammatory omega-6 fatty acids. Typically, Americans consume far too many omega-6’s and not nearly enough omega-3’s.
Magnesium is a cofactor for more than 300 enzymes in the body; it is important for blood-sugar regulation, and has a calming effect on the nervous system (Nadler 1995). Some evidence shows a link between magnesium deficiency and depression, and a recent, comprehensive review in the Journal of Medical Hypotheses suggests that magnesium supplementation is a viable approach for depressive symptoms..
A major hurdle for supplemental magnesium historically has been delivery into the brain. This is a barrier that has limited the ability of typical magnesium supplements to target conditions that arise from within the central nervous system such as depression and anxiety. However, in a recent scientific breakthrough, researchers collaborating from Beijing, Ontario, the University of Texas, and the Massachusetts Institute of Technology have developed a highly advanced form of supplemental magnesium called magnesium-L-threonate.
Magnesium-L-threonate was shown in multiple animal models to not only effectively penetrate deep into the brain, but also to trigger enhancements in learning and memory by optimizing neuronal communication and reinforcing brain structure in key areas of the cortex, the most advanced aspect of the human brain. Since magnesium-L-threonate is readily able to diffuse across the blood brain barrier, while other forms of magnesium are not, it appears to be the ideal form of supplemental magnesium for those with depression of other mood disorders.
Supporting Neurotransmitter Synthesis: Tryptophan and 5-HydroxyTryptophan (5-HTP)
L-tryptophan and 5-hydroxytryptophan (5-HTP) are immediate precursors to serotonin. L-tryptohan is essential for the brain to synthesize serotonin, and several studies have shown that acute tryptophan depletion can cause depression in humans. In fact, some foreign countries license L-tryptophan as an antidepressant.
In one study, healthy women given L-tryptophan for 14 days experienced increased recognition of happy faces and words, and decreased recognition of negative words. The research team concluded L-tryptophan had improved the study participants’ supply of serotonin in a manner similar to that of SSRIs. In another study of the effects of acute tryptophan depletion on healthy women and on patients with bulimia nervosa, both groups were given amino acid mixtures to decrease their plasma L-tryptophan levels. Both groups experienced an increase in depression. Other studies have found L-tryptophan depletion can lead to recurrence of depression in those who are in remission from depression or in those with seasonal depression.
Methylation (a biochemical building block process for producing neurotransmitters):
Methylation is a process in which a molecule passes a methyl group to another molecule. Methylation is essential to multiple functions in the body, including the production of neurotransmitters. One can supply raw materials to support methylation reactions by supplementing with S-adenosyl-methionine (SAMe) or by providing metabolic cofactors such as folate, vitamin B12, and vitamin B6. These nutrients are necessary for neurotransmitter production and have other regulating effects.
SAMe, which can be found in almost every tissue in the body, assists with production of creatine, glutathione, taurine, L-carnitine, and melatonin. SAMe can benefit depressed patients who do not respond to SSRIs. In a well-controlled, 6-week, double-blind trial, 73 subjects with treatment resistant depression were treated with an SSRI plus placebo, or an SSRI plus 1,600 mg SAMe daily. The group receiving the SAMe experienced significantly better response rates and remission compared to the placebo control group. Intriguingly, the group that received SAMe also displayed improved memory function over those receiving placebo. A smaller 6-week study revealed a response rate of 50% and a remission rate of 43% in subjects taking 800–1,600 mg a day of SAMe as an adjunct to their antidepressants.
Research shows that low blood levels of folate are associated with depression (Alpert 2000), and may also be predictive of poor response to antidepressant medication. Clinical trials have also demonstrated that folic acid both relieves depression on its own and enhances the effect of antidepressants. In one study, patients given 500 mcg folic acid daily in conjunction with fluoxetine experienced a significant improvement in depressive symptoms compared with patients receiving the antidepressant alone; women particularly benefited. Because relapse is associated with low serum folate, it is important to maintain folate supplementation for a year following a depressive episode.
The form of supplemental folate is important since a considerable portion of Americans may have a genetic polymorphism that impairs folate metabolism. In fact, mutations in the gene (MTHFR) that converts folic acid into the active 5-methyltetrahydrofolate (5-MTHF) are associated with depression (Lewis 2006). Therefore, taking supplemental 5-MTHFdirectly, which can cross the blood-brain barrier, may be more effective in supporting healthy neurotransmission and decreasing potentially neurotoxic homocysteine levels.
Vitamin B12 should always be measured in the event of depression (or any other psychological problems) as a vitamin B12 deficiency can be a reversible cause of various neuropsychiatric disorders. One should also consider whether a vegetarian diet or malabsorption due to celiac disease or gluten enteropathy is a factor in B12 deficiency.
Weaker digestion, reduced absorption of nutrients, and hypochlorhydria (inadequate stomach acid needed to break down proteins that contain vitamin B12) are common in the aging population and associated with a B12 deficiency; B12 levels should be tested in an older person with symptoms of depression. Evidence suggests that the methylcobalamin form of B12may have more beneficial metabolic effects than cyanocobalamin.
Vitamin B6 is a cofactor for the production of most neurotransmitters, but it is particularly important for serotonin synthesis (Baldewicz 2000). B6 levels are often low in women taking oral contraceptives and research has shown that B6 supplementation in these women can improve mood. For example, one study showed 22 women who had depression associated with oral contraceptive use and a B6 deficiency saw significant improvement in their symptoms with B6 supplementation (Adams et al 1973).
A more recent study examined blood levels of pyridoxal-5-phosphate (P5P), a metabolically active form of B6, in the blood of 251 elderly individuals living is Massachusetts. The investigators found that deficient levels of P5P doubled the likelihood of depression in this population. Accordingly, when dietary composition was assessed, those with higher daily B6 intakes were less likely to be depressed.
Blood sugar regulation and insulin resistance: Chromium and Green Coffee Extract
Recent data link increasing consumption of coffee with decreased risk of depression. In fact, this relationship proved to be dose-dependent, meaning that the more coffee study participants drank, the less likely depression would strike them. These findings are corroborated by a similar study conducted in 2010, which supports the link between increasing coffee consumption and decreased depression. Interestingly, this last trial was unable to link caffeine with depression risk, suggesting that other compounds in coffee may be responsible for the mood-elevating effect.
Conventional coffee preparation, which involves roasting the green coffee beans at high temperatures to attain the desired flavor profile, dramatically lowers levels of health-promoting coffee constituents called chlorogenic acids.
Chlorogenic acids have been shown in several studies to aid in controlling blood sugar levels; especially those glucose spikes which occur after a high-carbohydrate meal. In a 12-week study, consumption of chlorogenic acid-fortified instant coffee lead to a considerable reduction in body weight when compared to regular instant coffee.. As elevated glucose levels and excess body weight are common among depressives, chlorogenic acids may help combat some symptoms of depression tied to insulin resistance and irregularities in glucose metabolism.
Green coffee, the primary source of chlorogenic acids, cannot be consumed as a beverage due to its extremely bitter taste. Consuming a green coffee extract standardized to chlorogenic acids is an effective means of obtaining biologically active concentrations of chlorogenic acids.
The potential role of chlorogenic acids in mediating the mood boost associated with coffee consumption, and their thoroughly studied antihyperglycemic properties give rise to promising multimodal depression protection.
Chromium has been studied for its role in regulating blood sugar by facilitating the uptake of glucose into cells, and some research indicates that it may be beneficial in depression as well. In one case series of five patients with minor depression, chromium supplementation led to remission. Two other pilot studies found chromium picolinate supplementation benefited atypical depression. Finally, although not studied for seasonal depression, chromium may help regulate blood sugar and cravings for sugar and carbohydrates in relation to seasonal depression.
Antioxidant Effects: N-Acetyl-cysteine, Lipoic acid, vitamins C and E, and Selenium
One of the best-researched antioxidants for depression is N-acetyl cysteine (NAC). NAC is a precursor to glutathione, one of the body’s most powerful antioxidants. Research has found glutathione depletion and oxidative stress in people with bipolar depression. Two recent studies showed NAC is a safe and effective adjunctive treatment that improves depression in patients with bipolar disorder.
Although lipoic acid has not been well studied for depression, it is one of the most effective supplemental antioxidants, since it helps recycle other antioxidants, such as vitamin C (May 2010). It also may benefit blood sugar regulation and neurological function, as evidence shows it can help diabetic neuropathy.
In general, antioxidants may help buffer nerve cell damage in cases of chronic or recurrent depression, although they also serve other roles in brain health. For example, the antioxidant vitamin C is an important cofactor in the synthesis of serotonin, norepinephrine, and adrenal hormones that mediate stress. Vitamin E helps protect nerve cell membranes, and low selenium levels are associated with depression.
Curcumin is a phytoceutical derived from turmeric, a spice used often in preparation of Indian cuisine. It belongs to a class of compounds called polyphenols, which have been extensively studied and shown to exert an array of health benefits. One of the most intriguing properties of polyphenols, and curcumin in particular, is the ability to positively influence mood. Indeed, mounting evidence suggests curcumin might represent an important novel modality for the treatment of depression.
Curcumin appears to modulate several aspects of neurobiology involved in mood and behavior. Experimental evidence from an animal model of depression suggests curcumin can preserve levels of a protein important for healthy neuronal function (brain-derived neurotrophic factor [BDNF]) in a region of the brain called the amygdala, which is involved in mood regulation. Curcumin appears to manipulate neurotransmitter signaling as well. In another animal model, mice with neuropathy (who are prone to depression) were treated for 3 weeks with 45 mg/kg of curcumin twice daily (about 583 mg daily for an 80 kg adult human). While these mice normally exhibit depressive-like symptoms, curcumin treatment ameliorated this behavior. Interestingly, the researchers found that curcumin may have eased the rodent’s depression by altering serotonin and gamma-aminobutyric acid (GABA) signaling in their central nervous systems.
Curcumin also helps relieve pain, which may be helpful for some individuals with depression because pain, especially of chronic nature, is closely – and potentially causally – associated with depression. Other studies show that curcumin’s powerful anti-inflammatory properties may also underlie its ability to elevate mood. In an experiment in which rats were exposed to chronic stress for 21 days to induce depressive-like behavior, curcumin administration was shown to significantly reduce signs of depression. This study also showed that curcumin considerably eased inflammation by suppressing activation of nuclear factor-kappaB (NF-?B), a master regulator of inflammation; the researchers concluded that curcumin’s antidepressant effects were due in part to its anti-inflammatory action.
Evidence for a potent antidepressant effect of curcumin among animals has been partially confirmed in at least one human study. In a randomized, double-blind, placebo-controlled trial, 40 people with new-onset depression were treated with antidepressants Lexapro or Effexot together with either curcumin (500 mg per day) or placebo for 5 weeks. Researchers then tracked subjects’ depression severity using several standardized assessments. Although subjects in both groups experienced comparable relief of their depression, those who received curcumin tended to achieve faster relief than those who received a placebo.
A significant amount of animal data data indicate curcumin may be a powerful tool in the treatment of depression, and, as of the time of this writing, additional human studies are ongoing to assess its effects on mood. Finally – and perhaps most importantly – curcumin, unlike conventional antidepressant medications, has an excellent safety and side-effect profile.
St. John’s Wort
St. John’s wort (Hypericum perforatum) is a medicinal herb used to treat neurological and psychiatric disorders, including depression. Compared to a placebo, H. perforatum extract is more effective at targeting mild to moderate depression, and reducing symptoms and recurrence rate. Its effectiveness is considered comparable to antidepressant medications, but its actions are more complex.
St. John’s wort’s mechanism of action on depression is not entirely understood, even though it is one of the most researched herbs for depression. St. John’s wort has been shown to inhibit serotonin and norephinephrine reuptake, thus increasing their availability at the synapse. Other investigators found it influences dopamine and GABA activity. Its antidepressant qualities also can be linked to its antioxidant and anti-inflammatory properties that normalize an overactive hypothalamus-pituitary-adrenal axis and stress response.
While additional research is on-going to identify all of the anti-depressant mechanisms of action, experimental models and clinical trials alike have shown that treatment with St. John’s wort delivers positive response rates for mild to moderate depression.
Unfortunately, potential side effects associated with St. John’s Wort deprive many depressives of its benefits.
Growing evidence suggests that vitamin D significantly effects depression. This is not surprising in seasonal depression, since the skin synthesizes vitamin D in response to sunlight, which is less available in the winter. However, vitamin D has been found to play other roles in depression. For example, in a study of 7,358 patients age 50 and over with a cardiovascular diagnosis and no a history of depression, low vitamin D levels significantly increased the risk of developing depression.
Studies also find that vitamin D3 (cholecalciferol) supplementation can improve symptoms of depression. One well-controlled study of 441 overweight and obese participants showed an association between low vitamin D levels and depression. High dose vitamin D supplementation (20,000–40,000 IUs per week or 2,800–6,000 IUs per day) for one year improved mood. Another pilot study noted significant improvement in depression in six of nine women with low levels of vitamin D upon supplementation.
Vitamin D’s effectiveness may be related to the high prevalence of vitamin-D deficiency in the general population, its importance in blood-sugar regulation, and its importance in overall regulation of genetic activity.
Zinc is a trace element known to help regulate the nervous system and may be specifically related to depression. Increasing evidence shows that decreased blood levels of zinc are associated with depression, and, in depressed subjects, lower levels of zinc are associated with worse depression. One pilot study of 20 depressed patients also showed that 25 mg a day of zinc augmented benefits of antidepressant medication.
Animal studies show that antidepressants and electroconvulsive shock treatments change zinc concentrations in areas of the brain associated with depression. In further animal research, zinc also was shown to enhance antidepressant effects of imipramine and influence serotonin levels and activity in several brain regions.
Inositol levels in the brain and cerebrospinal fluid were found to be lower in subjects with depression. One well-controlled trial showed that taking 12 grams a day of inositol helped relieve symptoms in 39 patients with depression.
Further research on bipolar depression suggests beneficial influences of inositol. A well-controlled but small trial of 17 participants with bipolar depression showed varied responses. Four of nine patients experienced significant improvement with inositol supplementation compared to zero of eight who took a placebo.
Inositol, a second-messenger precursor, has important cellular communication functions in the nervous system. Interestingly, inositol is also involved with insulin signaling and function. It therefore may have more of an effect on overweight or obese individuals, as well as those who are insulin resistant, such as those with metabolic syndrome or women with polycystic ovarian syndrome (PCOS). These findings require further research and replication.
There are many causes of depression, and efficient relief often requires addressing multiple neurochemical and metabolic imbalances that may underlie mood disturbances. The nutrients listed in this protocol are categorized according to their evidence-based mechanisms of action in brain health and mood regulation.
Many of these suggestions may serve as adjuvants to conventional therapies for depression. Always consult a qualified healthcare professional before combining any supplements with an antidepressant medication.
Broad-Range Nervous System Effects
- Fish oil (with olive polyphenols): 1400 mg EPA and 1000 mg DHA daily
- Magnesium L-Threonate: 2000 mg daily (supplying 144 mg elemental magnesium)
Supporting Neurotransmitter Synthesis
- 5-hyroxytryptophan (5-HTP): 50 – 200 mg daily
- Tryptophan: 1000 – 2000 mg daily
Supporting Methylation Reactions
- S-Adenosylmethionine (SAMe): 400 – 1200 mg daily
- L-methylfolate: 1000 mcg daily
- Vitamin B12 (as methylcobalamin): 1000 – 8000 mcg daily
- Vitamin B6 (as pyridoxal 5-phosphate): 100 mg daily
Supporting Blood Sugar Regulation
- Chromium: 500 mcg daily
- Green Coffee Bean extract (standardized 50% to chlorogenic acid): 400 mg before each meal, up to three times daily.
- N-Acetyl-cysteine: 600 – 1200 mg daily
- R-lipoic acid: 300 – 600 mg daily
- Vitamin C: 1000 – 2000 mg daily
- Vitamin E (as high gamma tocopherol mix): 350 mg daily
- Selenium (as Se-methylselenocysteine): 200 mcg daily
Supporting Mitochondrial Health
- Coenzyme Q10 (as ubiquinol): 100 – 200 mg daily
- Pyrroloquinoline quinine (PQQ): 10 – 20 mg daily
- Acetyl-L-Carnitine: 1000 – 2000 mg daily
Men and women with depression should consider restoring their hormone concentrations to youthful levels with the use of natural bioidentical hormones. More information is available in the Male Hormone Restoration and Female Hormone Restoration protocols. A natural, over-the-counter hormone men and women should consider optimizing is:
- DHEA: 15 – 50 mg daily for women or 25 – 75 mg daily for men
Miscellaneous Sources of Symptom Relief
- Vitamin D: 5000 – 8000 IU daily (depending on blood test results)
- Zinc: 30 mg daily
- Inositol: 2000 – 10?000 mg daily
- Comprehensive multivitamin / multinutrient formula: Per label instructions
- St. John’s Wort; standardized extract: 300 – 600 mg daily
- Curcumin (as highly absorbed phospholipid blend): 630 mg daily