L-Methylfolate Benefits (depression, etc.) + Side Effects

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Methylfolate is crucial to DNA synthesis and detoxifying homocysteine. What role does it play in pregnancy, development, and mental health? Find out here.

Folate, otherwise known as vitamin B9, is one of the 13 essential vitamins. Vitamins come in different forms called vitamers that often need to be converted in the body to active forms of the vitamin. The active form of folate in the body is L-methylfolate, also known as levomefolic acid, which can cross both cell membranes and the blood-brain barrier [1].

A critical role of L-methylfolate is to act as a regulator of a class of neurotransmitters called monoamines. The three different neurotransmitters it helps make are [2]:

Folate can’t be synthesized by the body, so it must be ingested either through food or supplements [3].

The synthetic form of folate is folic acid, which can be found in fortified foods such as bread and cereals, and multivitamins [2, 4].

Dihydrofolate is the dietary form of folate and can be found in green vegetables, egg yolk, legumes, grains, nuts, some fruits, yeast, and organ meats like liver and kidneys [2, 4].

Both folic acid and dihydrofolate are converted into L-methylfolate in the body by a specific enzyme. It is then transported into the brain where it increases the production of the three neurotransmitters mentioned above [2].

Unmetabolized folic acid has been associated with an increased incidence of prostate cancer, lower cognitive test scores, and smaller red blood cells. Some researchers and health professionals have therefore started recommending L-methylfolate supplements rather than folic acid [5, 6].

Although many people take L-methylfolate supplements, much of the naturally ingested L-methylfolate actually comes in the form of different folates such as folic acid and dihydrofolate [2, 4].

The conversion of these folates to L-methylfolate is crucial because L-methylfolate can cross the blood-brain barrier, while the other forms of folate can’t [4].

L-methylfolate is typically regulated as a medical food. Some doctors may prescribe it for the purpose of slowing the cognitive decline that is seen in many mental disorders, including Alzheimer’s, mania, and depression.

Many of these disorders are linked to mutations in the gene that produce the enzyme that converts folate into L-methylfolate, 5, 10-methylenetetrahydrofolate (MTHFR) [7, 8, 9, 4].

Mutations in MTHFR can lead to decreased methylfolate production. Mutations in MTHFR are relatively common, and there are up to 30 different kinds of MTHFR mutation variations [4].

Methylfolate is responsible for many methylation reactions all throughout the body. Methylation reactions occur when methylfolate donates a methyl group (three hydrogens bonded to one carbon atom) to another molecule [4].

Methylation reactions are crucial for processes such as cell division and DNA and RNA synthesis. Methylation of DNA and RNA plays a crucial role in epigenetics, the mechanism by which gene activity changes without modifying the DNA sequence [10].

L-Methylfolate is involved in:

Homocysteine is a toxic amino acid that is particularly damaging to blood vessels (endothelial cells). High levels of homocysteine lead to increased inflammation and risk of coronary heart disease [4].

L-methylfolate methylates homocysteine into the less-toxic methionine, an essential amino acid [4].

According to the FDA, L-methylfolate is a naturally occurring folate found in foods and is generally recognized as safe. It has been approved as a food additive, but not as a treatment for any medical purpose or health claim. Talk to your doctor before supplementing.

Folate deficiency during pregnancy is dangerous and can lead to disorders in both the fetus and the mother. Because of the importance of supplementation, the U.S. government began mandating the addition of more folic acid into grain products (140µg/100g) in January 1998 [3, 11].

Folic acid is a more common supplement than L-methylfolate. However, new research in women both with and without MTHFR variants suggests that L-methylfolate could be more effective. In a study of 144 women of childbearing age, those who took L-methylfolate experienced a greater increase of folate levels in their red blood cells than those who took folic acid [12].

Neural Tube Defects (NTD)

Supplementation with folic acid or L-methylfolate helps prevent neural tube defects, which are defects of the brain, spine, and spinal cord [12].

Pregnant women with a family history of NTD are recommended to take 5mg of folate (usually as folic acid) daily, while all other pregnant women are typically advised to take 0.4-1mg daily [12].

Anemia

Pregnant women usually have reduced hemoglobin (protein that carries oxygen in the blood) levels, which leads to anemia in 5% of pregnancies [3].

In one retrospective study, 58 pregnant women taking prenatal supplements along with L-methylfolate had significantly higher hemoglobin levels at the time of delivery than 54 women taking prenatal supplements with folic acid [13].

Preterm Birth

Low blood folate levels have been linked to shorter pregnancy times [3].

A study of 34,480 women found that supplementing with folate for longer than one year significantly decreased the chances of preterm birth. The length of folate supplementation (> 1 year) was equally as important as supplementing itself [3].

Other

Supplementing with folate has also been shown to reduce risks of other pregnancy problems such as heart defects and orofacial clefts, which are openings that may form in the mouth and lip [14, 15].

One study of 123 patients with either depression or schizophrenia found that a third of them had folate deficiencies. Patients with folate deficiencies were given either methylfolate or placebo. The patients given methylfolate improved significantly compared to placebo both clinically and socially, especially in mood, and the difference in improvements increased with time [9].

In another study of 68 depression patients who did not respond to conventional antidepressants (selective serotonin reuptake inhibitors, or SSRIs), 15 mg/day of L-methylfolate was given for 12 months. Of the 68 patients, 26 recovered completely from their depression and 35 experienced a reduction in the severity of their depression (remission), leaving only 7 who did not improve [16].

None of the patients who had a full recovery experienced a relapse or recurrence of their symptoms during the trial [16].

In another study, 147 patients given only SSRIs were three times more likely to become hospitalized than patients given SSRIs plus L-methylfolate supplements [17].

Depression is a complex condition, and many drugs and supplements might work for some people but not others. Some researchers believe that L-methylfolate supplementation could be more effective in depression patients with these traits [2]:

When homocysteine is converted to methionine by L-methylfolate, S-adenosylmethionine (SAM-e) concentrations rise. SAM-e is responsible for donating methyl groups to fat molecules that line our cell membranes and in the formation of the neurotransmitter serotonin [4].

Potential Benefits (Possibly Effective)

These potential benefits have been studied in humans and produced promising results. However, some of these studies used folic acid supplements rather than L-methylfolate, leading to a lack of specificity and a source of doubt. Further trials of L-methylfolate, specifically, will be required to confirm any benefit.

As always, talk to your doctor before supplementing, and never use L-methylfolate in place of something your doctor prescribes.

In a study of 91 schizophrenic patients, low blood folate was associated with the severity of negative symptoms of schizophrenia. The authors suggested that poor diet and cigarette smoking could be responsible for the low folate [18].

In a study (DB-RCT) of 140 schizophrenic patients, only those given folic acid with vitamin B12 supplementation improved negative symptoms considerably. Treatment response was further associated with a mutation in the FOLH1 gene, which is one of the genes responsible for metabolizing methylfolate [19].

All the patients in the previously mentioned study had been on antischizophrenic drugs for six months prior or longer, but had shown no improvements in symptoms [19].

In another study of 35 schizophrenic patients, L-methylfolate not only improved symptoms but also produced beneficial physiological changes in the brain [20].

The patients given L-methylfolate supplements showed increased cortical thickness in the medial prefrontal cortex (mPFC), which was correlated to a partial restoration of structure and function of the mPFC [20].

The medial orbitofrontal cortex (mOFC), which normally deactivates during tasks requiring working memory, is dysfunctional in schizophrenic patients. The patients receiving L-methylfolate supplementation showed increased deactivation [20].

Schizophrenia is a highly complex and poorly understood disorder. Further studies will be required to determine the role of folate supplementation and FOLH1 gene mutations in people with schizophrenia [19].

People with Alzheimer’s disease are more likely to have reduced folate levels compared to healthy people. Researchers are therefore investigating whether L-methylfolate supplements can improve symptoms in those patients [21].

Alzheimer’s disease is an inflammatory condition which is linked to higher levels of tumor necrosis factor (TNF)-α, an inflammatory molecule, and amyloid beta plaques in the brain. In one study of 121 patients newly diagnosed with Alzheimer’s, folic acid significantly reduced levels of TNF-α and amyloid beta [21].

In a recent clinical trial of 30 Alzheimer’s and dementia patients with high homocysteine, a supplement including L-methylfolate (alongside methylcobalamin and NAC) reduced brain deterioration in the hippocampus and cortex of the brain [7].

The authors suggested that the conversion of homocysteine may have slowed brain deterioration and improved cognitive function [7].

Additional trials are required to determine whether L-methylfolate (or other forms of folate) might be helpful to Alzheimer’s patients with or without high homocysteine.

Other Potential Benefits with Insufficient Evidence

These potential benefits have been studied in humans, but either the evidence comes from extremely small studies, or available results are contradictory. Talk to your doctor before using L-methylfolate in these conditions.

Bipolar disorder is characterized by periods of depression and mania.

The Montgomery Asberg Depression Rating Scale (MADRS) is used to measure the degree of depression in patients with a higher score number being worse [8].

Mania is a state of heightened arousal, elevated mood, and increased energy. The Young Mania Rating Scale (YMRS) is used to score mania with higher numbers signifying worse mania [8].

In a study of 10 patients with bipolar depression, L-methylfolate in combination with conventional treatment reduced the average MADRS score from 23.4 to 13.9 and the average YMRS from 3.2 to 2.7 [8].

Six out of the 10 patients showed at least a 50% improvement in MADRS score and the other four experienced a reduction in the severity of their depression (remission) [8].

Larger and more robust human trials will be required to determine whether L-methylfolate is helpful to people with bipolar disorder.

In a study of 29 autistic children, folic acid supplementation improved sociability and cognitive and verbal symptoms. However, excess folic acid supplementation during pregnancy has been associated with increased rates of autism in offspring, leading some researchers to suggest that unmetabolized folic acid could be a risk factor for autism [22, 23].

Mutations in the gene encoding the enzyme 5,10-methylenetetrahydrofolate (MTHFR) disrupt the enzyme’s ability to convert folic acid into L-methylfolate. L-methylfolate decreased symptoms of aggressive and disruptive behavior in an autistic child with an MTHFR C667T mutation [24].

Further studies are required to determine whether any form of folate is helpful or harmful in people (especially children) with autism.

Areas for Future Research

Researchers are currently investigating L-methylfolate in other contexts, but no clinical evidence supports the use of L-methylfolate for any of the conditions listed in this section. Below is a summary of the existing cell-based research, which should guide further investigational efforts. However, the studies listed below should not be interpreted as supportive of any health benefit.

T cells are the part of the immune system that provides short-term defense against pathogens. A cell study showed that folate deficiency led to decreased production of T-cells [25].

Increasing folate levels increased the T-cell levels to normal levels [25].

Other studies have shown that deficiencies in folate also lead to decreased responses of T-cells and antibodies to certain pathogens. This ultimately leads to decreased resistance to infections [26].

Requirements & Dietary Sources

Folate, or vitamin B9, is considered an essential nutrient. As with most nutrients, the best and most available sources of folate is from food. The NIH recommends that adults get 400 mcg of folate per day, increasing to 600 mcg for pregnant and lactating mothers [27].

Liver is by far the best dietary source of folate. Other good sources include green vegetables like spinach, asparagus, and brussels sprouts [27].

Folate is a required nutrient, and L-methylfolate is generally recognized as safe. Some reported side effects of L-methylfolate supplementation include [8]:

Overconsumption of L-methylfolate may also mask vitamin B12 deficiencies. It’s important to talk to your doctor about supplementation to make sure your lab markers are normal [3].

Many of the commercial L-methylfolate supplements contain between 5,000 mcg (5 mg) and 1,000 mcg (1 mg). However, many studies have used doses of up to 15 mg to see intended effects [9].

Consult your physician to determine the appropriate supplement dose for you.

1) Drugs that May Reduce Folate Absorption

Certain drugs can decrease folate levels leading to decreased L-methylfolate concentrations in the brain due to interfering with absorption. Some examples are listed below [4]:

A study done on 36 children taking Carbamazepine and 30 children taking Valproate showed that these medications reduced folic acid levels in the blood significantly [28].

The loss of folic acid led to significantly higher levels of homocysteine in the children taking Valproate and Carbamazepine [28].

2) Methotrexate

Methotrexate has been used to treat psoriasis, which is a disease that causes the formation of red patches on the skin with silver plaques and scales, for over 40 years [29].

However, methotrexate works by inhibiting dihydrofolate reductase (DHFR), an enzyme that metabolizes folic acid. Therefore, L-methylfolate supplementation can work to counteract the mechanisms by which methotrexate heals [29].

A case study on one patient taking both methotrexate for his psoriasis and L-methylfolate for his depression showed the patient developed psoriatic lesions after taking L-methylfolate. Only when the patient stopped taking methotrexate did the lesions disappear [29].

1) Antidepressants

A study comparing L-methylfolate plus selective serotonin reuptake inhibitors (SSRI, a common antidepressant) therapy (95 patients) with just SSRI therapy (147 patients) showed that adding L-methylfolate greatly enhanced results [17].

For instance, discontinuation rates for L-methylfolate plus SSRI were 17.9% compared to 34% for only SSRI therapy [17].

By 60 days, a major improvement was seen in up to 18.5% of patients on L-methylfolate plus SSRI patients while only 7% of patients on just SSRI showed improvements [17].

The time it took until major improvements showed was 177 days for the patients on L-methylfolate plus SSRI compared to 231 days for patients solely on SSRI [17].

The combined therapy also showed that patients were more likely to adhere to the therapy, and fewer people refused treatment due to lower rates of adverse events [17].

2) Vitamin B12 and N-acetylcysteine

In a study of 67 patients with Alzheimer’s disease, L-methylfolate supplementation with vitamin B12 and N-acetylcysteine significantly slowed deterioration in the brain. The degree to which these compounds interact (and potentially synergize) with each other is not yet clear [7].

3) Cholinesterase Inhibitors (ChI)

Cholinesterase inhibitors prevent the enzyme cholinesterase from breaking down the neurotransmitter acetylcholine.

In a study (DB-RCT) of 57 Alzheimer’s patients, folic acid supplementation appeared to improve the effects of ChI therapy. The patients given both folic acid and ChI therapy significantly improved in performing daily living activities and in social behavior compared to patients only given ChI therapy [30].

This effect has not been investigated with L-methylfolate specifically.

4) Donepezil

Folic acid supplementation along with Donepezil (used to treat Alzheimer’s disease) and natrium diethyldithiocarbamate trihydrate (NDDCT) greatly improved symptoms in those with vascular dementia [31].

The increased effects were seen in the areas of learning, memory, and endothelial dysfunction [31].

The enzyme 5,10-methylenetetrahydrofolate (MTHFR) is responsible for the conversion of folate or folic acid into L-methylfolate. Mutations in the gene responsible for MTHFR creation lead to decreased L-methylfolate production from its precursors [4].

Humans have two copies of each gene and different forms of the same gene are called alleles.

There are up to 30 different kinds of mutations in the MTHFR gene. Up to 60% of Americans carry at least one allele with a mutation in the MTHFR gene (heterozygous).

One common mutation is called C677T and it is prevalent in up to 10% of the white people and up to 22% of the Hispanics and Mediterranean populations. Having one allele with this mutation decreases MTHFR activity by up to 35%, while having two alleles with this mutation (homozygous) decreases activity by 70% [32, 19].

One male patient suffering from depression, mania, and obsessive-compulsive disorder (OCD) was screened and found with an MTHFR C677T mutation. Common medications were tried and failed to produce results. Only after L-methylfolate supplementation did the male patient showcase improvements [33].

Another common mutation called A1298C also reduces MTHFR activity [34]. Individuals with two alleles with this mutation show a 68% reduced activity in the MTHFR enzyme [12].

Patients suffering from schizophrenia and bipolar disorder are even more likely than depressed patients to have MTHFR mutations [35].

Researchers are studying L-methylfolate as an alternative to folic acid because it has the potential to bypass these relatively common MTHFR mutations and increase methylation reactions throughout the body [4].

Mutations in the FOLH1 gene can also result in reduced folate levels due to impaired absorption of folate in the gut [36].

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Vitamin B12

Vitamin B12 is part of the Vitamin B complex. It is considered to be a “Painkilling vitamin”. It helps DNA production, cardiovascular support, and energy metabolism. In this post, learn more about Vitamin B12, its functions, causes of deficiencies, as well as foods and other sources so you can better incorporate B12 into your life.

Vitamin B12 is a very important marker to monitor, especially if you haven’t been leading the best lifestyle or you have known chronic health issues.

Vitamin B12, also referred to as cobalamin, is a water-soluble vitamin [1].

It contributes to the successful synthesis of DNA, the normal functioning of the nervous system, and the production of energy [2].

The liver is the main site of storage of vitamin B12 in the human body [3]. Humans can obtain vitamin B from dietary sources, fortified foods, and supplements [4, 5, 6].

It can take the form of cyano-, hydroxyl, methyl, and deoxy adenosyl-cobalamin [7].

Cyanocobalamin, the most stable and unnatural form of vitamin B12, is most commonly used in supplements and does not have a direct cofactor role in cellular metabolism.

The most biologically significant forms of vitamin B12 are methylcobalamin and coenzyme B12 (5’-deoxy-5’-adenosylcobalamin) [8, 9].

Vitamin B12 was considered the “Painkilling Vitamin” in some countries as far back as the 1950s [10].

The normal range for vitamin B12 is between 200 and 900 nanograms per milliliter (ng/mL).

In this case, however, your lab result may be in the reference range, but not actually be in the optimal range. Vitamin B12 even in the ‘normal’ range can be unhealthy and indicate that certain processes in the body aren’t optimal.

Cobalamin helps break down methylmalonic acid (MMA) [11] and homocysteine – hence, high levels of MMA or homocysteine in the blood may indicate a B12 deficiency. Some studies say this is even a better indicator of B12 status than direct B12 measurement [12].

One study in 94 women found that vitamin B12 levels lower than 250 mg/dL increased risk by 3X the likelihood of having a child with birth defects [13].

Methylcobalamin, a form of Vitamin B12, reduces the clinical symptoms in legs such as paresthesia (an abnormal sensation like tingling or pricking), burning pains, and spontaneous pain [14].

In one study, methylcobalamin significantly improved symptoms, such as pain and prickling sensation, in patients with neck pain [15].

Intramuscular cobalamin injection is effective in alleviating low back pain in patients with no nutritional deficiencies [16].

Cobalamin provides effective pain management for mouth ulcers [17].

Methylcobalamin treatment reduces pain symptoms in neuralgia, diabetic neuropathy, and lower back pain [18, 19, 20].

Methylcobalamin (MeCbl) is the most effectively taken form of vitamin B12 in neuronal organelles [10].

Cobalamin may have a role in the prevention of disorders of brain development and mood disorders as well as Alzheimer’s and vascular dementia in the elderly [23].

Supplementation of cobalamin is useful in neuronal regeneration. It also repairs the negative effects of ischemia on neurons [24].

A study on rats with sciatic nerve injuries supports the treatment of peripheral nerve injuries with Cobalamin [25].

B12 also increases the regeneration of axons and promotes neuronal repair [26, 27, 28].

Cobalamin treatment improves sleep-wake rhythm disorders in human subjects [29, 30].

It may increase the light sensitivity of circadian rhythms due to decreased melatonin levels [31].

It’s not normal to struggle falling asleep and wake up in the morning feeling more tired than when you went to bed. Biohacking Insomnia attacks sleep issues from every angle including limbic system repair, hormone levels, and circadian rhythm retraining.

In a randomized trial performed on patients with depression and low normal cobalamin levels, cobalamin supplementation improved depressive symptoms [32].

Studies have found that prolonged consumption (several weeks to years) may decrease the risk of depression relapse and the onset of clinically significant symptoms in people at risk [33].

Methyl B12 suppresses cytokine production of T lymphocytes in cells and is speculated to do the same in patients with rheumatoid arthritis [34].

Topical cobalamin is a new therapeutic option in atopic dermatitis. It is well-tolerable and has low safety risks for both adults and children [35, 36].

One randomized clinical trial states that oral cobalamin supplementation with 250 μg/day throughout pregnancy and early lactation elevates maternal, fetal, and breast milk vitamin B12 levels [37].

Higher homocysteine and decreased B12 levels have been associated with an increased risk of macular degeneration [38].

One study involved 5,442 women at high risk of cardiovascular disease aged 40 or older, who had been taking B6/B9/B12 for 7 years.

The study found a 34 – 41% decreased risk of macular degeneration when supplementing with B6/B9/B12 may reduce the risk of macular degeneration [39].

B12 (Cobalamin) leads to the production of S-Adenosyl-Methionine SAM, which increases methylation [40, 41, 42, 43, 44].

Only fortified nutritional yeast contains vitamin B12.

Vitamin B12 Deficiencies

The long-term consequences of less severe B12 deficiency are not fully known but may include adverse effects on pregnancy, vascular, cognitive, bone and eye health [54].

Methylcobalamin increases nerve conduction, myelin regeneration, neuron regeneration, and inhibiting pain transmission [21, 10, 22, 10].

B12 deficiency in women is associated with infertility and miscarriage [55].

B12 deficiency causes excess homocysteine, which is a proven risk factor for cardiovascular disease [56]. Individuals with B12 deficiency have a higher prevalence of cardiovascular risk factors such as heart failure, stroke, and diabetes [57].

Deficiency of B12 inhibits melanin transfer between melanocytes and keratinocytes, which may cause darkening of the skin. 19% of subjects in one clinical trial manifested skin darkening resulting from cobalamin deficiency [58, 59].

Vitamin B12 plays an essential role in the production of red blood cells and low red blood cells can indicate a B12 deficiency [60, 61]. Weakness and fatigue can result if your red blood cells are low since you are not getting enough oxygen to tissues.

Since vitamin B12 is important in producing myelin, a deficiency can cause psychiatric and cognitive problems and pins & needles. In one study with 141 patients, 28% of people who had psychiatric symptoms from B12 deficiency didn’t have any signs of anemia [62].

Low levels of B12 have been linked to depression [33] and Alzheimer’s disease and other types of cognitive impairment [63].

Studies have found that prolonged consumption (several weeks to years) may decrease the risk of depression relapse and the onset of clinically significant symptoms in people at risk [33].

B12 deficiency can cause neuropathy or nerve pain [64], either as a result of a lack of oxygen to the nerves or from myelin destruction.

In this study, every patient treated with B12 had an improvement in psychiatric problems (39 of 39). They also improved various blood markers, as well as a 50% decrease in methylmalonic acid and/or homocysteine [62].

In one 7-year-old boy, B12 deficiency from a vegan diet resulted in neurological symptoms [65].

Multiple studies show that B12 deficiency in the elderly can increase the risk of weakness, frailty, and disability, and increase hospital stay [66, 67, 54, 68].

With regard to bone health, multiple studies show that B12 deficiency can increase the risk of bone fracture and is associated with lower bone mass [54, 69].

In 4 people who didn’t have cognitive symptoms or anemia, a swollen and inflamed tongue with lesions was found to be an early sign of vitamin B12 deficiency [70].

Although rare, vitamin B12 deficiency can cause blurred vision or eye pain. This can occur when an untreated B12 deficiency results in damage to the optic nerve [71].

About 6% of people in the US aged 60 or older are clinically vitamin B12 deficient, while about 20% have technically “normal” levels (148 – 221 pmol/L), but are far from optimal [72].

Vitamin B12 deficiency increases with age, from about 1 in 20 among people aged 65 – 74 years to 1 in 10 or even greater among people aged 75 years or greater [67].

Pregnant women require higher levels of B12 to prevent birth defects (over 300 mg/dL [13]).

Infants born to B12 deficient mothers or receiving deficient amounts of animal-sourced foods are susceptible to deficiency between the ages of 6 – 12 months [74].

Patients with type 2 diabetes who are prescribed Metformin may be at risk for cobalamin deficiency [75].

Proton pump inhibitors or Histamine 2 receptor blockers (Zantac, Tagamet) may lead to b12 deficiency, as a result of poorer B12 absorption [76, 77].

Hormonal birth control (oral contraception and DMPA) usage among female subjects reduced B12 levels [78].

Genes (notably TCN2) related to B12 deficiency are associated with autoimmune gastritis [79].

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About the Author

Joe Cohen won the genetic lottery of bad genes. As a kid, he suffered from inflammation, brain fog, fatigue, digestive problems, anxiety, depression, and other issues that were poorly understood in both conventional and alternative medicine.Frustrated by the lack of good information and tools, Joe decided to embark on a journey of self-experimentation and self-learning to improve his health--something that has since become known as “biohacking”. With thousands of experiments and pubmed articles under his belt, Joe founded SelfHacked, the resource that was missing when he needed it. SelfHacked now gets millions of monthly readers.Joe is a thriving entrepreneur, author and speaker. He is the CEO of SelfHacked, SelfDecode and LabTestAnalyzer.His mission is to help people gain access to the most up-to-date, unbiased, and science-based ways to optimize their health.

Joe has been studying health sciences for 17 years and has read over 30,000 PubMed articles. He's given consultations to over 1000 people who have sought his health advice. After completing the pre-med requirements at university, he founded SelfHacked because he wanted to make a big impact in improving global health. He's written hundreds of science posts, multiple books on improving health, and speaks at various health conferences. He's keen on building a brain-trust of top scientists who will improve the level of accuracy of health content on the web. He's also founded SelfDecode and LabTestAnalyzer, popular genetic and lab software tools to improve health.

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