Key takeaways:
~ Trace minerals, including copper, iron, lithium, magnesium, manganese, and zinc, can influence mood and cognitive function.
~ Genetic variants can interact with your need for these minerals, increasing or decreasing the amount you need.
~ Understanding your genetic variants is just one part of the picture, but it can be a starting point for knowing what to test or what to try first.
Trace Minerals affect Mood, Focus, and Cognitive Function
Minerals, known as trace elements or micronutrients, play an essential role in brain development as well as neurotransmitter levels and cognitive function in adults.
The idea of looking at your genes and knowing that you need more of a certain mineral to optimize mood is tantalizing. The reality, though, is that genetic variants may be more of a fine-tuning or just part of the picture. Often, understanding your genes can give you a starting point, but you may find that you need to experiment with diet and/or supplements to see what works for you.
How to use this information:
The goal of this article is not to give a protocol or prescription. Instead, you’ll take away an understanding of the research and genetic connections, and then you can experiment to figure out what is optimal for you.
Keep in mind that you may not need to take a supplement forever. You may find that once you’ve restored your levels, you don’t need it as often – or that dialing in your dietary intake may be sufficient.
Talk with your doctor if you have any medical questions before starting any supplements, including mineral supplements.
Testing your mineral levels:
To know your serum levels of minerals, a blood test is needed. You can ask your doctor to order it for you, or in most states in the US, you can order your own lab tests from multiple online sources.
Genetic variants in genes related to mineral absorption or transport can help you know what to test or try first.
Let’s dive into the research on magnesium, copper, zinc, lithium, manganese, and iron – along with the genetic connections to neurocognitive function.
Magnesium: Depression, ADHD, Cognitive Function
Studies link magnesium supplementation to improving different neurocognitive and psychological conditions, and you may see online headlines claiming that magnesium can cure depression, ADHD, etc. However, magnesium is unlikely to be a panacea for everyone.
Genetic variants can point to whether you are more likely to be deficient in magnesium, especially if your diet is borderline to low in this mineral. The only way to know your levels for sure is to get a blood test done, but adding in more magnesium-rich foods or a low-dose supplemental magnesium is a low-cost intervention with few drawbacks.
Clinical trials on magnesium and cognitive disorders:
Depression:
Multiple studies show that magnesium may help reduce depression.[ref] Here’s a sample:
- In patients who had been hospitalized for Covid, magnesium supplementation (300 mg/day) reduced depression scores and enhanced quality of life.[ref]
- Another clinical trial looked at the effect of magnesium alone or magnesium plus B6 and showed that both treatments significantly improved depression and anxiety scores during the first four weeks.[ref]
- A systematic review of seven clinical trials showed that magnesium reduced depression scores on average for adults.[ref]
ADHD and emotional conduct:
A randomized, double blind, placebo-controlled clinical trial looked at the effect of magnesium (6mg/kg/day) plus vitamin D in children with ADHD. The results showed that 8 weeks of supplementation significantly reduced emotional and conduct problems compared to placebo.[ref]
Magnesium L-threonate and adult ADHD:
A clinical trial in adults with ADHD found that half of the participants had an improvement in symptoms with 12 weeks of supplemental magnesium l-threonate.[ref]
Magnesium orotate plus probiotics and CoQ10 for depression:
A double-blind placebo-controlled clinical trial looked at the effect of magnesium plus probiotics (Lactobacillus and Bifidobacterium) with CoQ10 on major depressive disorder. The study found that the combination was more effective than a placebo for reducing depressive disorder symptoms.[ref]
Cognitive function in aging:
A number of studies show that low magnesium is linked to neurodegeneration and cognitive dysfunction in aging. More is not always better, though. Studies point to a U-shaped curve, with hypermagnesmia (excessively high magnesium) also increasing the risk of cognitive decline.[ref]
Proton pump inhibitor (PPIs), magnesium, depression, and genetics:
PPIs are commonly prescribed for GERD or heartburn, but they can cause decreased magnesium absorption, especially when combined with a TRPM6 gene variant (below). Studies show that PPIs increase the relative risk of depression, with higher doses linked to a 2-fold increase in risk.[ref][ref]
RDA and dietary sources of magnesium:
The US RDA for magnesium is 420 mg/day for adult males and 320 mg/day for women. Good dietary sources of magnesium include pumpkin seeds, chia seeds, almonds, spinach, cashews, peanuts, and black beans. [ref]
What happens with too much magnesium? Well, an excess of magnesium is what is used to prep for a colonoscopy… You get the picture.
Magnesium Neurocognitive Connections Report:
Below are genetic variants that may connect mood disorders or cognitive changes to low magnesium levels. Keep in mind that these variants do not cause a specific disorder, but rather can lead to low magnesium and increased risk (especially when combined with a diet low in magnesium).
Read the full article on magnesium here.
CNNM2 genetic variants:
The CNNM2 gene encodes a transporter in the kidneys that is important in magnesium reabsorption and maintaining normal Mg levels.[ref] Genetic variants in this gene are linked to changes in magnesium levels, which influence brain development and blood pressure.
Check your genetic data for rs7914558 (23andMe v5; AncestryDNA)
- G/G: decreased gray matter (on average)[ref], possibly altered neural systems relevant to social cognition, increased risk of schizophrenia[ref]
- A/G: common genotype
- A/A: typical
Members: Your genotype for rs7914558 is —
TRPM6 variants:
TRPM6 encodes the ion transporter that regulates magnesium uptake in the intestines and impacts magnesium reabsorption in the kidneys. While magnesium can be taken up passively, the TRPM6 transporter is important for fine-tuning magnesium intake.
Check your genetic data for rs3750425 (23andMe v4, v5; AncestryDNA):
- C/C: typical
- C/T: lower serum magnesium levels; increased risk of hypomagnesia with proton pump inhibitors; increased risk of type 2 diabetes if magnesium intake is low
- T/T: lower serum magnesium levels[ref]; increased risk of hypomagnesia with proton pump inhibitors[ref; increased risk of type 2 diabetes if magnesium intake is low[ref]
Members: Your genotype for rs3750425 is —
Check your genetic data for rs2274924 (23andMe v4; AncestryDNA):
- C/C: lower magnesium levels on average; increased susceptibility to epilepsy post-stroke[ref], increased risk of hypomagnesia with proton pump inhibitors[ref]; increased risk of type 2 diabetes if magnesium intake is low[ref] increased risk of gestational diabetes with low magnesium intake[ref]
- C/T: lower magnesium levels, on average; increased risk of hypomagnesia with proton pump inhibitors;
- T/T: typical
Members: Your genotype for rs2274924 is —
Check your genetic data for rs121912625 (23andMe v5; AncestryDNA):
- A/G: rare mutation linked to hypomagnesia[ref]
- G/G: typical
Members: Your genotype for rs121912625 is —
Copper: Neurotransmitters, Bipolar, Schizophrenia, and Depression
Copper (Cu) is a trace element found in all tissues of the body. It is essential for life, but toxic in excess.
When it comes to mental health and cognitive function, it isn’t as straightforward as “more copper = good”. Instead, copper levels are found to be low in some individuals with depression and high in the serum of people with schizophrenia. It’s thought that in schizophrenia, higher plasma copper levels could indicate impaired transport into the cells.
Copper is involved in neurotransmitter levels through several key enzymes:[ref][ref]
- Dopamine-β-hydroxylase is a copper-containing enzyme that converts dopamine to norepinephrine
- Tyrosinase is a copper-containing enzyme that oxidizes dopamine to form neuromelanin
- GABA-A receptor activity is
Balancing oxidative stress also plays a role in mood disorders in multiple ways. Copper is involved in antioxidant defences as it is incorporated into Cu/Zn-superoxide dismutase (SOD1).
ATP production in the mitochondria is also integral to brain function. Part of the electron transport chain in the mitochondria (cytochrome c oxidase) contains a copper ion.
Copper levels are strongly regulated in the body, since high levels of copper can cause cell death. Copper ( Cu+) is transported into cells by SLC31A1. In the cytoplasma, part of the copper will bind to glutathione, and the rest may be used in the synthesis of copper-containing enzymes or for SOD1 to detoxify ROS. Copper can also be transported from the cytoplasm into mitochondria for use in cytochrome C oxidase (ATP production).[ref]
Ceruloplasmin is a copper-binding protein. 75-90% of serum copper is bound to ceruloplasmin, with the rest circulating as free copper. High levels of free copper can indicate Wilson’s disease or other copper pathology.[ref]
Balance is key with copper.
Different studies show opposite results when it comes to whether high or low copper is associated with mood disorders.
Higher levels of serum copper are associated with increased depressive symptoms.[ref] This is especially true when combined with low folate. Researchers think it is a synergistic increase: High serum copper and low folate doubled the relative risk of depression.[ref] Excess copper can cause oxidative stress through redox reactions.[ref]
However, several other studies show that a higher dietary copper intake is associated with a reduced risk of depression.[ref]
In schizophrenia, copper deficits have been found in specific brain regions. Proteomics studies show disrupted copper transport (CTR1) in the brain.[ref]
This points to a balance of copper being needed — and to a difference between using serum levels compared to questionnaires about the diet. Dietary questionnaires may not be a good representation of intake due to variations in getting copper from water pipes in homes. In areas with water with a lower pH, copper is more likely to leach into the water.[ref]
RDA, dietary sources, and normal levels:
The RDA for copper for adults is 900 mcg/day. Copper-rich foods include liver, oysters, chocolate, potatoes with skin, shiitake mushrooms, cashews, crab, sunflower seeds, chickpeas, and tofu. According to the NIH, ” Normal serum concentrations are 10–25 mcmol/L (63.5–158.9 mcg/dL) for copper and 180–400 mg/L for CP”. [ref]
Copper Neurocognitive Connections Report:
ATP7B gene: Copper transporter responsible for maintaining copper levels in the body. In the liver, ATP7B facilitates copper being incorporated into ceruloplasmin (copper-binding protein), and also transports copper to the bile for excretion. In Wilson’s disease, the loss of ATP7B activity causes excess copper accumulation in cells, leading to inflammation, liver problems, depression, and psychotic episodes.[ref]
Check your genetic data for rs1061472 K832R (23andMe v4, v5; AncestryDNA):
- C/C: common variant; higher levels of unbound copper[ref] exposure to higher copper levels increases inattentiveness in children[ref]
- C/T: typical
- T/T: typical
Members: Your genotype for rs1061472 is —
Check your genetic data for rs1801243 (23andMe v4; AncestryDNA):
- A/A: typical
- A/C: typical
- C/C: exposure to higher copper levels increases inattentiveness in children[ref]
Members: Your genotype for rs1801243 is —
SLC31A1 gene: encodes copper transporter 1 (CTR1)
Check your genetic data for rs10981694 (23andMe v5):
- G/G: likely increased copper transport; more likely to have toxicity from cisplatin (chemotherapy for lung cancer)[ref] increased relative risk of lung cancer[ref]
- G/T: likely increased copper transport; more likely to have toxicity from cisplatin (chemotherapy for lung cancer)[ref] increased relative risk of lung cancer[ref]
- T/T: typical
Members: Your genotype for rs10981694 is —
DBH gene: encodes dopamine beta-hydroxylase, a copper-dependent enzyme that catalyzes the conversion of dopamine to norepinephrine. Higher dopamine can increase motivation and drive, but it can also cause restlessness, agitation, difficulties in concentrating, and, at very high levels, paranoia or psychosis
One connection between dopamine and copper is that copper deficiency can exacerbate the effect of genetically lower DBH expression. In people on copper-chelator drugs (disulfiram), the combination with low DBH expression increased the risk of paranoia and psychosis when combined with dopamine stimulation (cocaine).[ref][ref]
Check your genetic data for rs1611115 1021C/T or C-970T (23andMe v4, v5; AncestryDNA):
- T/T: lower DBH expression (higher dopamine); increased relative risk of schizophrenia and bipolar disorder[ref]; higher neuroticism and novelty seeking[ref]; increased risk of paranoia and psychosis with copper-binding drug (disulfram), especially in conjunction with cocaine[ref]
- C/T: somewhat lower DBH expression (somewhat higher dopamine); increased risk of paranoia and psychosis with copper-binding drug (disulfram), especially in conjunction with cocaine
- C/C: typical
Members: Your genotype for rs1611115 is —
Wilson’s disease mutations:
Wilson’s disease is caused by rare mutations in ATP7B, resulting in an accumulation of copper in the body. If you have the ATP7B mutations below, read the full article on Wilson’s Disease here.
| Gene | RS ID | Your Genotype | Effect Allele | Effect Allele Frequency | Notes About Effect Allele |
|---|---|---|---|---|---|
| ATP7B | rs76151636 | -- | T | 0.001 | mutation that can cause Wilson's disease (2 copies needed) |
| ATP7B | rs28942074 | -- | A | 0.00005 | mutation that can cause Wilson's disease (2 copies needed) |
| ATP7B | rs137853283 | -- | T | 0.0001 | mutation that can cause Wilson's disease (2 copies needed) |
| ATP7B | rs72552255 | -- | A | 0.0001 | mutation that can cause Wilson's disease (2 copies needed) |
| ATP7B | rs60431989 | -- | G | 0 | mutation that can cause Wilson's disease (2 copies needed) |
| ATP7B | rs28942076 | -- | T | 0 | mutation that can cause Wilson's disease (2 copies needed) |
| SOD2 | rs4880 | -- | A | 0.51 | A/A: earlier age of onset of Wilson’s disease symptoms in males |
| MTHFR | rs1801133 | -- | A | 0.33 | earlier age of onset of Wilson’s disease symptoms |
| MTHFR | rs1801131 | -- | G | 0.3 | earlier age of onset of Wilson’s disease symptoms |
Manganese: Behavioral Disorders, Schizophrenia, and Neurodegenerative Disorders
Manganese is a micronutrient that is essential in trace amounts but has negative effects at high levels.
Manganese-dependent enzymes can affect neurotransmitter levels:
- Glutamine Synthetase: This enzyme catalyzes the ATP-dependent conversion of glutamate and ammonia to form glutamine. Glutamine is an important amino acid. It is part of protein synthesis and purine synthesis, and it can also be used by cells for energy production (conversion to alpha-ketoglutarate).
Manganese also influences mitochondrial function and oxidative stress in cells:
- Manganese superoxide dismutase (MnSOD) is an enzyme produced in cells that acts as an antioxidant. In short, cells produce reactive oxygen species (ROS) when they make ATP for energy. The amount of ROS in cells must be kept low to prevent oxidative stress, and MnSOD helps regulate ROS levels. Specifically, MnSOD converts superoxide anion radicals, which are the major source of cellular ROS, to hydrogen peroxide and oxygen in the mitochondria.[ref]
Balance is key with manganese:
Carriers of mutations that cause extremely low levels of manganese have a higher risk of schizophrenia, which is also linked to glutamate regulation in the brain and oxidative stress.[ref]
Higher manganese levels are associated with neurocognitive symptoms such as: [ref][ref]
- Behavioral disorders in children
- Unstable emotional behavior
- Neurodegenerative disorders
RDA and dietary sources:
The recommended adequate intake for manganese is 1.8 mg/day for adult women (slightly more if pregnant or breastfeeding) and 2.3 mg/day for men. Manganese-rich foods include mussels, hazelnuts, pecans, brown rice, oysters, clams, and chickpeas. [ref]
Manganese Neurocognitive Connections Report:
Read the full article on manganese here.
SLC30A1 gene: encodes a Mn efflux transporter that balances manganese levels by moving it out of the body. Rare mutations in this gene can lead to manganese accumulation and toxicity in the brain.[ref][ref][ref]
Check your genetic data for rs2275707 (23andMe v4; AncestryDNA):
- A/A: typical
- A/C: increased blood manganese concentration, reduced transport into cells; increased relative risk of lower cognitive performance and increased behavioral problems in children
- C/C: increased blood manganese concentration, reduced transport into cells[ref] increased relative risk of lower cognitive performance and increased behavioral problems in children[ref]
Members: Your genotype for rs2275707 is —.
SLC39A8 gene: encodes a cation influx transporter SLC39A8 (ZIP8), which has a high affinity for Mn but can also transport iron, zinc, and cadmium. SLC39A8 facilitates manganese uptake.[ref]
Check your genetic data for rs13107325 A391T (23andMe v4; AncestryDNA):
- C/C: typical
- C/T: ~ 15% lower average blood Mn concentration, lower risk of behavioral problems and hyperactivity in children
- T/T: ~ 50% lower average blood Mn concentration, lower risk of behavioral problems and hyperactivity in children and adolescents[ref][ref][ref] increased relative risk of schizophrenia[ref][ref] increased risk of Crohn’s due to alterations in intestinal barrier[ref][ref]
Members: Your genotype for rs13107325 is —.
Lithium: Depression, Aggression, and Alzheimer’s
Lithium is a naturally occurring mineral found in foods at concentrations dependent upon the mineral content of the soil. It is also an essential element that people need – in small amounts. High amounts of lithium are toxic.[ref]
We get roughly 3 -4 mg of lithium per day naturally in our food and water, although this varies depending on where you live and where your food was grown.
Lithium has long been known to have a positive effect on mood for some people. It is traditionally used at high doses in the lithium carbonate form for bipolar disorder as a prescription medication. Lithium orotate as a supplement is available in low doses, more along the lines of what you get from mineral-rich water and foods.
Several studies show that areas with higher lithium levels in their drinking water have lower levels of depression and decreased aggression.
- A meta-analysis of studies on lithium in water showed that suicide rates were >50% lower in areas with higher lithium in the drinking water.[ref] Note that not all studies show this connection, but the majority do.
- Another study found that homicide rates were lower in areas with higher levels of lithium in the water supply.[ref]
ADHD and lithium orotate:
Some clinicians recommend low-dose lithium orotate for ADHD.[ref] In adults with ADHD, a study using high-dose lithium found that it was as effective as methylphenidate in reducing irritability, aggressive outbursts, and more.[ref] In animals, lithium increases working memory.[ref]
Cognitive function in aging:
Low-dose lithium orotate has been studied in multiple clinical trials for preventing cognitive decline in aging. A recent study explains why and how lithium is important for brain health as we age. The researchers found that lithium is sequestered in the amyloid-beta deposits, reducing its bioavailability in the rest of the brain. In addition, lithium deficiency also causes a 3 to 4-fold increase in tau tangles.[ref]
Lithium Orotate Neurocognitive Connections
Read the full article on lithium orotate here.
Genetic variants that impact lithium carbonate (prescription lithium):
Direct studies looking at lithium orotate and genetic variants are lacking, so studies here are on another form, lithium carbonate, which is used for bipolar disorder. Not everyone responds to lithium for bipolar disorder, and genetic variants play a large role in response.
While biologically plausible, these same genetic connections may not hold entirely true for low-dose lithium orotate since the amount of lithium in the prescription medication is orders of magnitude higher than supplemental lithium orotate.
ACCN1 gene: codes for a cation channel in neurons that is responsive to sodium, potassium, and lithium
Check your genetic data for rs11869731 (23andMe v5):
- C/C: may be more likely to respond to lithium for bipolar disorder[ref][ref]
- C/G: typical response
- G/G: typical response
Members: Your genotype for rs11869731 is —.
CACNG2 gene: calcium channel gamma-2 subunit
Check your genetic data for rs2284018 (23andMe v4, v5):
- C/C: more likely to respond to lithium for bipolar disorder[ref][ref]
- C/T: more likely to respond to lithium for bipolar disorder
- T/T: typical response rate
Members: Your genotype for rs2284018 is —.
BDNF gene: codes for brain-derived neurotrophic factor, which is important in the way neurotransmitters work and in neuroplasticity.
Check your genetic data for rs6265 Val66Met (23andMe v4, v5; AncestryDNA):
- T/T: decreased BDNF[ref] referred to in studies as Met/Met; introversion, resilient to adverse events, a quicker decline in Alzheimer’s[ref][ref][ref] may have a better response to lithium carbonate for bipolar disorder[ref]
- C/T: somewhat decreased BDNF, referred to as Val/Met;
- C/C: typical BDNF, referred to as Val/Val
Members: Your genotype for rs6265 is —.
GADL1 gene: encodes glutamate decarboxylase-like protein 1
Check your genetic data for rs17026688 (23andMe v4; AncestryDNA):
- C/C: Typical
- C/T: more likely to respond to lithium carbonate for bipolar disorder
- T/T: more likely to respond to lithium carbonate for bipolar disorder[ref]
Members: Your genotype for rs17026688 is —.
Clinicians also connect lithium orotate to helping move vitamin B12 into cells. Stacking lithium with B12 may be helpful for some people. Before starting methylB12, be sure to read more about the types of vitamin B12 and COMT here.
Zinc: Depression, Addiction, Anxiety, and PMS
Zinc is an essential trace mineral that is integral to the way your cells function. Researchers estimate that over 3000 different cellular functions rely on zinc.[ref][ref]
Mental health and cognitive function:
Studies show that low levels of zinc can increase the risk of mental health problems, such as depression. A meta-analysis showed that people with depression are more likely to have lower zinc levels, and intervention studies show that increasing zinc consumption alleviates depression in people.[ref]
Anxiety:
A systematic review looked at 9 studies on zinc and anxiety. The consensus was that patients with anxiety had lower levels of serum zinc, as compared to a healthy control group.[ref]
Reduced addiction relapse:
A clinical trial in patients with opioid addiction showed that zinc supplementation combined with methadone was more effective than methadone alone. Zinc supplementation helped to reduce drug cravings and decreased depression and anxiety.[ref]
Hormonal mood changes (PMS):
A study involving women with PMS found that 50 mg/day of elemental zinc during the second half of their cycle reduced PMS severity scores (somewhat). [ref]
Stack zinc with:
Quercetin and EGCG act as zinc ionophores. This means that it helps to move zinc into the cells.[ref]
RDA and dietary sources:
The recommended dietary allowance (RDA) for zinc is 11 mg/day for men and 8 mg/day for women. The upper daily limit (UL) for zinc is set at 40mg/day. Longer-term supplementation at levels higher than this could result in adverse events for some people.[ref] Good dietary sources of zinc include oysters, beef, crab, lobster, and pork.
Zinc Neurocognitive Connections Report:
Read the full article on zinc.
SLC39A2 gene:
The SLC39A2 gene codes for zinc transporter ZIP2, controlling zinc influx into the cytoplasm of the cell.
Inflammation is strongly linked to increased relative risk of depression, so the connection here is that zinc may help to reduce elevated inflammatory cytokine levels.
Check your genetic data for rs2234632 (AncestryDNA only)
- G/G: typical
- G/T: higher inflammatory cytokines without zinc supplements; zinc supplementation works to reduce inflammation; likely impaired zinc transport into the cell
- T/T: higher inflammatory cytokines without zinc supplements; zinc supplementation works here to reduce inflammation[ref][ref]; likely impaired zinc transport into the cell
Members: Your genotype for rs2234632 is —.
Iron: Depression, Autism, Alzheimer’s, and Parkinson’s
Iron is essential for life since it is involved in the transport of oxygen throughout the body. However, it is also a highly reactive metal, so levels of iron are tightly regulated in the body.
High iron:
Excess iron causes oxidative stress in cells, and if iron levels are too high, excess iron will be stored in organs, such as the liver and brain. Hemochromatosis is a genetic disease caused by mutations in HFE and other genes that cause an excess of iron to be absorbed from food.
Psychiatric conditions:
Oxidative stress in the brain can cause depression. A study in the late 90s pointed to the role of iron overload in treatment-resistant psychiatric patients. Since then, multiple studies, including genetic studies, have shown the connection between high iron and depression or other mood disorders.[ref][ref]
Brain iron accumulation is thought to contribute to autism, bipolar disorder, Alzheimer’s, and Parkinson’s disease. For people with neurodegeneration, there’s now a classification for psychiatric symptoms caused by neurodegeneration with brain iron accumulation (NBIA).[ref]
Low iron:
Iron is essential in the right amounts. For menstruating women who have low iron levels, supplementing with enough iron to bring their levels up improves symptoms of depression and anxiety.[ref]
RDA and dietary sources:
The RDA for iron is 8 mg/day for men and 18 mg/day for women before menopause (8 mg/day post-menopause). Dietary sources of iron include oysters, white beans, beef liver, lentils, spinach, chocolate, sardines, and chickpeas.[ref]
Cereals and bread often have iron added to them. This form of free iron that is added to fortified foods can be more easily absorbed and can be a problem for people with HFE mutations.
Iron Neurocognitive Connections Report:
More details in the full article on iron – please read if you have either variant below.
HFE gene: codes for a protein that controls how iron is absorbed in the intestines.[ref] Mutations here can cause hemochromatosis or iron overload. This interaction with increased iron can cause lower manganese levels.
If you have the HFE variants, please read the full Hemochromatosis article.
Check your genetic data for rs1800562 C282Y (23andMe v4, v5; AncestryDNA):
- A/A: two copies of the C282Y variant, most common cause of hereditary hemochromatosis, highest ferritin levels; lower serum manganese levels[ref][ref]
- A/G: one copy of C282Y, increased ferritin levels, hemochromatosis possible but less likely[ref], check to see if combined with H63D (below) – combo increases the risk of hemochromatosis; lower serum manganese levels[ref][ref]
- G/G: typical
Members: Your genotype for rs1800562 is —.
Check your genetic data for rs1799945 H63D (23andMe v4, v5; AncestryDNA):
- G/G: two copies of the H63D variant increase the risk of (mild) hemochromatosis, and increased ferritin levels; linked to lower serum manganese levels[ref]
- C/G: one copy of H63D, possibly higher ferritin levels, can cause hemochromatosis in conjunction with one copy of C282Y (above); linked to lower serum manganese levels[ref]
- C/C: typical
Members: Your genotype for rs1799945 is —.
Conclusion:
Genetic variants make us all unique, including our need for individual micronutrients. Dialing in your micronutrient intake may help give you the baseline you need for optimal neurocognitive function.
Keep in mind that your need for different nutrients can fluctuate depending on stress, environmental exposure, and lifestyle factors. You may find a supplemental micronutrient very effective at certain times, but it may not be something that you need to take long-term. If you are going to supplement with a mineral for a long period of time, talk with your doctor about how often you should test your levels to make sure you’re in the right range. If you are looking for professional help with testing and optimizing, check out the Genetic Lifehacks PRO members directory.
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