How light at night could double your risk of cancer.

The World Health Organization listed ‘light at night’ as a possible carcinogen in 2007. That is an eye-opening statement for something that affects almost all of us. From streetlights to the lamp in the living room, from accent garden lighting to the glow of TV’s and cell phone… artificial light at night is truly ubiquitous.

An often stated fact is that 80% of people in North America cannot see the milky way at night.  What was more surprising to me was that the Milky Way was supposed to be visible!  Who knew?  Oh, wait – people who don’t have light pollution know…

So how can light possibly be a carcinogen? Will turning on the TV or a light in the living room after dinner suddenly cause cancer?  Let me start with two recent, contradictory studies, and then I’ll get into the science of why I think that artificial light at night is a fundamental health problem. 

A few weeks ago a study was released that looked into breast cancer incidences and light at night in Israel.  The study used spectral imaging – a satellite mapping method that looks at the color spectrum of light – to investigate a link between wavelengths of light and breast cancer.  This was based on animal studies that showed that shorter wavelengths (the blue end of the light spectrum) were associated with increased breast cancer. The researchers factored in the socio-economic impact, age, ethnicity, and other environmental factors that increase the risk of breast cancer.  The study showed that rather than all light at night being associated with increased breast cancer risk, only areas with more light in the blue wavelengths were at an increased risk. [ref]

Not all studies agree that light at night impacts cancer risk, of course.  Another study published in February 2018 showed that exposure to light at age 20 didn’t increase the risk of breast cancer. I did see a few flaws in the study…  The participants were women in their mid-40’s who were asked to report on how much light they were exposed to at night when they were 20.[ref] I’m a woman in my mid-40’s, and I have no idea what my light exposure at night was when I was 20.  I probably would have said it was dark at night.  In fact, up until a year or so ago when I finally installed blackout curtains, I had no idea what sleeping in the true dark really felt like.

Studying light exposure at night is difficult and hard to prove causation for cancer. The majority of the world is exposed to more and more light at night. Ubiquitous. While hormone-related cancers have risen over the last fifty years,  a number of other things we are all exposed to – like endocrine disrupting chemicals – can also be linked to cancer.

Let me dig into the research a little more and explain why light at night is most likely a carcinogen, and then I’ll put it into perspective, showing how large the risk is so that you can decide if it is something you should actually do something about.

Melatonin and cancer:
Melatonin, which most people think of as ‘the sleep hormone’, rises at night and falls during the daytime. This is a circadian rhythm that is maintained in most animals, and it is governed by light hitting the retina of the eye. Even in nocturnal animals, melatonin will rise at night.

Melatonin, though, is not really a just sleep hormone. In addition to circadian signaling, recent research shows that melatonin acts as an antioxidant, helping to repair our cells at night. While we sleep, our cells go into rest and repair mode, cleaning up the waste from the active period during the day.

Two factors govern melatonin: light during the day and absence of light at night.

Melatonin levels are affected by the amount of light (specifically in the blue wavelengths) that you get during the daytime.  A June 2018 animal study on liver cancer found that increasing blue wavelengths (465-485) during the day increased nighttime melatonin levels by 7x compared to the animals kept under standard fluorescent lighting. The animals exposed to the blue-enriched light also had markedly reduced tumor growth. The daytime blue light exposure and increased nighttime melatonin decreased the Warburg Effect, which is the shift to glycolytic metabolisms that cancer cells exhibit.[ref] Other studies have shown similar increases in melatonin and decreases in tumors (prostate, oral, breast).[ref][ref][ref]

The rise in melatonin at night is governed by the lessening of the blue light hitting our eyes in the evening hours. As the sun heads towards the horizon, we get more of the red end of the light spectrum. The golden hour.  In studies, the rising of melatonin levels is referred to as ‘dim light melatonin onset’.

While suppressing melatonin with lots of blue light during the day is good, at night, we need melatonin levels to rise so that our body can clear out bad cells and fight off cancer.

Studies over the last twenty plus years have made it clear that light at night (dim or bright) causes a decrease in melatonin levels, and animal studies show without much doubt that the decreased nighttime melatonin levels increase the risk of certain types of cancer. [ref][ref][ref][ref][ref]

Human studies for cancer are based on looking at the environmental factors (in this case either light at night or lack of light during the day) and then correlating them with an increase in risk. We, of course, can’t do human trials to intentionally test a condition to cause cancer, so there always seems to be a little wiggle room to be hopeful and say “maybe light doesn’t affect humans like it does all other mammals”. The overwhelming evidence of a link between light at night and cancer, though, really means that we need to pull our heads out of the sand on this topic and take a real look at the impact on our health.

Night shift workers have an increased risk of breast cancer:
Evidence from studying shift workers (mainly nurses) showed varying results for the increased risk of breast cancer.  One large study found a 79% increase in breast cancer risk for women working the night shift for 20 years, [ref]   while another look at the combined data from the Nurses Health Studies found that for women exposed at younger ages to night shift work (light at night) there was a more than doubled risk of breast cancer.  [ref] But not all studies show such a large risk, with one estimating only a 7 – 21% increase in risk. [ref]

What about the risk from general light at night (street lights, lights at home)?

It turns out that you don’t have to work the night shift to have an increased risk of cancer due to light at night.  A California study of over 100,000 women found a 34% increased risk of breast cancer for premenopausal women exposed to higher amounts of light at night.[ref]

There are quite a few smaller studies on breast cancer and light at night with similar findings to the larger ones – with a few interesting tidbits thrown in.

One study found a 51% increased risk with higher ambient light at night.[ref]   It also found that sleeping longer (thus more melatonin) cut the risk of breast cancer in half.

Closing the shutters at night (shutting out the streetlights) was also associated with a significant decrease in cancer risk.[ref]

Why does a dim light at night matter?  You have your eyes closed when you sleep, right.

A study from a few years ago tested a light device to see if they could shift melatonin levels while the participants were asleep.  The researchers used sleep masks with different colored led lights built into them; the lights turned on for two seconds every minute for an hour while the study participants slept. The results showed that blue wavelengths through their closed eyelids had an effect on melatonin – actually shifting the time that melatonin onset began the following night. [ref]

How much light is too much?  The answer may surprise you…  Even 0.2 lux (way less than a nightlight) was found to affect cancer rates in rats.[ref]   Most studies on dim light at night use 5 lux, which would be about the amount of light from having a nightlight out in the hall near your bedroom.  To put this in perspective, on a sunny day the outdoor illuminance can be as high as 120,000 lux, and a cloudy day is about 1,000 lux. Contrast this with a moon-lit night which ranges from .002 lux to .25 lux (quarter moon vs full moon).

Beyond melatonin:
In addition to affecting melatonin levels, light at night also increases cancer risk through activation of stress hormones. [ref]  The connection between an increased risk for hormonal cancers and salivary cortisol levels has been well established, and disruption to the normal circadian rhythm of cortisol is linked doubling the risk of death in breast cancer. [ref]

So there is a bit of a double whammy here: light at night decreases melatonin (cancer preventative) and increases stress hormone levels (cancer causing).

Quantifying the risk:
So after all of the studies (and there are hundreds more than I’ve referenced here), what is the consensus for the cancer risk from light at night?  The World Health Organization and the American Medical Association both place light at night as a probable carcinogen.  Probable, though, is a word with wiggle room.

The problem with quantifying the impact of light at night is that it is pretty much everywhere.  There are a few darker spots left, though, around the world. A  study looking at artificial light levels in protected or natural areas (such as forests, conservation areas, etc)  in 158 different countries and compared the cancer incidences to areas with high light. The results of the study, when all confounders were taken into account, showed that colorectal, prostate and breast cancer risk increased by up to 35% with light at night. [ref]

What does a 35% or 79% or 2-fold increase (depending on the study!) in breast cancer risk really mean? The lifetime risk in the US of breast cancer for women is 1 in 8, with the risk increasing with age. [ref]  So a 35% increase is going to change that risk to about 1 in 6, while a 2-fold increase would increase the lifetime risk to 1 in 4.  Putting this into perspective against other known breast cancer carcinogens: hormone replacement therapy increases the risk of breast cancer by 75% (~1 in 5) [ref]; BRCA1/2 gene mutations can increase risk of breast cancer to about 1 in 2.[ref]  So light at night is not as risky as carrying the BRCA mutations, but possibly as risky or riskier than hormone replacement therapy.

Why is no one else talking about this?
There are a few articles here and there in the mainstream media on the topic of cancer and light at night, mostly when a new study comes out. And there are a few health gurus that have started talking about the impact of light at night.  The problem is that the topic gets lost in the swirl…

This topic isn’t sexy or exciting, and, quite frankly, blocking blue light at night is inconvenient. No one can make a profit by telling people to turn off their lights and go to bed.  No one wants to listen to that – sounds like just some hippie-dippie wacko stuff.  But there is more research on this topic than pretty much anything else that I’ve blogged about. The science is real. And it is time to take it seriously.


Simplest: get as much light as possible during the day.  Go outside in the morning when you get up.  Have your cuppa tea or coffee outdoors.  A recent study also showed that blue light emitting bulbs during the day help increase the production of melatonin at night. [ref]

Also simple, but sometimes kind of geeky/not cool: wear blue-blocking glasses in the evening starting a couple of hours before bedtime. Many studies show that wearing blue-blocking glasses in the evening increase melatonin production and sleep quality and quantity. [ref][ref]

Alternative to blue blocking glasses: shut off all your lights at night and go back to using candlelight.  Yeah — probably not realistic.  So get yourself some blue blocking glasses and join the dork club.

Curtains: Get some curtains and sleep in the dark. True dark is needed, so get blackout curtains or perhaps curtains over blackout shades.  Also get rid of all the little lights in your bedroom from LED indicator lights.  A little bit of black electrical tape will block them out.

A cell study found that curcumin in combination with melatonin killed bladder cancer cells.  So perhaps taking curcumin at night before bed would increase its cancer prevention ability.[ref]

Resveratrol, in combo with melatonin, was somewhat effective in reducing tumors in rats. Taking resveratrol at night may boost its benefits.[ref] Resveratrol and melatonin both boost sirtuin 1, an enzyme vital to cellular function and longevity.[ref]

Melatonin pills:
If melatonin is so great, why not just take a pill instead of producing it yourself naturally? Melatonin as an adjuvant to chemotherapy has been shown to be helpful and something to talk with your oncologist about if you are currently doing chemo.[ref][ref]  The problem with just popping a melatonin pill for the rest of us is that a big single dose isn’t what your body needs/expects. The natural rise and fall of melatonin that your body produces without light disruption is just plainly better, so your better option is to block out the blue light. Additionally, people react to the hormone differently, and your natural production of melatonin may decrease with supplementation.

Food sources of melatonin:
Almost all plants contain small amounts of melatonin which acts as an antioxidant in the plant. Pineapple, oranges, and bananas all have been shown to significantly increase serum melatonin levels.[ref] The flip side of this is that you really shouldn’t eat at night due to a circadian drop in insulin sensitivity.

Genetic variants that increase susceptibility to Lyme disease

Lyme disease is caused by being bitten by a tick that carries the bacterium Borrelia burgdorferi  in North America or other Borrelia species in Europe.  General symptoms after being bitten can include a bulls-eye rash, fever, headache, pain, and general malaise. The majority of people recover after a few weeks, but some have symptoms (neurological, cardiovascular, fatigue, arthritis) that can last for months or even years.

Whether you are one of the ones who recover quickly or have chronic symptoms including joint pain or arthritis may be due to genetic variants that you carry.

Immune Response:
The innate immune system reacts quickly to pathogens, giving us the initial inflammatory response to fight off bacterial invaders.  One part of the innate immune system is the toll-like receptor (TLR) family, which helps the body to recognize specific bacteria, like Borrelia.

The simplified picture is that the innate immune system recognizes the Borrelia bacteria, raises an alarm bringing in inflammatory molecules to destroy it. It is the front line of the body’s army, quick to rise and fight a short battle.

Part of our individuality is found in different genetic variants in our innate immune system. It makes sense for a population to carry different variants – some may be better at fighting off leprosy, others good at surviving cholera.  While variation is good on whole, for an individual, though, it can end up causing increased susceptibility to a pathogen like Borrelia.

TLR1 (Toll-like Receptor 1) -Check your Genetic Variants:

One variant in TLR1, rs5743618 or T1805G, causes a decreased TLR1 functionality for people carrying the CC genotype.  This is an advantage when it comes to leprosy and cuts the risk of severity. [ref] But when it comes to Lyme disease, this variant is linked to an increased risk of ‘antibiotic refractory Lyme arthritis’ which basically means that joints still ache after taking several rounds of antibiotics.[ref]

The C variant for rs5743618 is found in about 50% of the Caucasian population, less than 10% of African populations, and is rarely found in Asian populations. [ref]

Check your 23andMe results for rs5743618 (v4, v5)

  • CC: 1.9x more likely to have antibiotic-refractory Lyme arthritis (but better off if you get leprosy)
  • AC: normal Lyme risk
  • AA: normal Lyme risk

There is another (uncommon) TLR2 genetic variant that is not covered by 23andMe testing. It is interesting because it cuts a person’s risk of Lyme disease by more than half and reduces the risk of long-term effects from Lyme even more substantially.[ref] This again shows the impact that our genetic variants in our immune system can have on our susceptibility to diseases.

HLA-DRB1 gene:

The HLA genes code for another part of our innate immune system known as the major histocompatibility complex. One variant, HLA-DRB1 *0401 has been linked to a greater susceptibility to antibiotic-resistant Lyme arthritis as well as being a risk factor for rheumatoid arthritis.[ref][ref][ref][ref]

So why am I going on about the link to rheumatoid arthritis, an autoimmune condition? There have been quite a few different studies over the past 20 years looking at the link between Borrelia infection and subsequent autoimmune diseases. There doesn’t seem to be a smoking gun study that definitively shows Borrelia causing autoimmune diseases (that I could find), but an interesting 2017 study looked at patients with Lyme arthritis who were diagnosed with autoimmune joint diseases within 4 months of getting Lyme.  The study results showed: “Most systemic autoimmune patients had positive tests for B. burgdorferi IgG antibodies by ELISA, but they had significantly lower titers and lower frequencies of Lyme-associated autoantibodies than LA patients. Prior to our evaluation, the patients often received additional antibiotics for presumed Lyme arthritis without benefit. We prescribed anti-inflammatory therapies, most commonly disease modifying anti-rheumatic drugs (DMARDs), resulting in improvement.” [ref]

HLA-DRB1 *0401

Check your 23andMe results for rs660895 (v4, v5):

  • GG: increased risk of Lyme arthritis, rheumatoid arthritis.
  • AG: increased risk of rheumatoid arthritis
  • AA: normal risk


Other factors affecting Lyme:

A study found that age is a factor in susceptibility to Lyme with elderly people likely to have a less vigorous immune response to the pathogen. The study also found that BMI, gender, vitamin D levels, and previous exposure to Borrelia had no effect on Lyme susceptibility.[ref]


Antibiotics are, of course, the first line of defense against Borrelia. Your doctor can give you more information on the effective antibiotics.

Below are some herbal remedies that are often recommended for chronic Lyme symptoms that persist after antibiotic treatment:

Stevia, an herbal sweetener, has been shown in the lab to kill Borrelia about as well as antibiotics do.[ref] I question whether this holds true in people rather than just in Petri dishes. But if you like stevia, it is probably a safe bet to use it when you have Lyme disease and it may help.

Andrographis paniculata is an Asian herb used in traditional medicine for respiratory infections and other ailments. It is recommended as an herbal remedy (combined with other herbs) for chronic Lyme disease.  While I didn’t find any studies on its effectiveness against Borrelia, there are quite a few studies on it for other diseases.  Studies have found it to be somewhat effective in the treatment of ulcerative colitis,  changing TH1/TH17 immune response, decreasing fatigue from MS, and as an antibiotic. [ref][ref][ref][ref]

Cat’s Claw (Uncaria tomentosa) is a traditional Peruvian herbal medicine that is often suggested for Lyme disease.  Again, I didn’t find any studies specifically showing that Cat’s Claw was effective for chronic Lyme disease symptoms. Studies do show that it is an antiviral and immunomodulator and that it may be effective for Dengue fever. Other studies show it affecting TNF-alpha and IL-1B levels in the immune response.[ref][ref][ref] You can get Cat’s Claw on Amazon or at most health food stores.

Japanese Knotweed (Polygonum multiflorum) is traditional Chinese herbal medicine sometimes recommended for Lyme. No Lyme specific studies, but there is a very good review of the effectiveness and safety of knotweed for a variety of ailments. Two constituents of knotweed are resveratrol and emodin.[ref]

Emodin, found in knotweed (above), is an anthraquinone that has been shown in a cell study to be effective against Borrelia.[ref] It is also found in rhubarb and is what causes the ‘gastrointestinal effects’ from eating too much rhubarb at once. Another source for emodin is cascara sagrada (also a laxative). There are quite a few studies on emodin, and it is possibly effective as an antimicrobial and as an anticancer agent. Studies also show that long-term, high doses may not be completely safe — so read up on it and know what you are getting into before you go overboard on this one.[ref] [ref]

All in all, there isn’t a ton of research on herbal remedies for chronic Lyme disease, even though there is a lot of discussion on various websites touting their effectiveness (and sometimes selling the products).  My guess is that emodin may be the most effective constituent of some of the herbal remedies.  Rhubarb pie with some stevia?

Dads matter: MTHFR variants in fathers affect miscarriage risk

There are quite a few studies showing that women carrying certain MTHFR variant combinations are at a somewhat higher risk for miscarriage, but I recently ran across a study that added a new twist to the topic.  It turns out that the father’s MTHFR variants can also play a role in recurrent miscarriages.

The study from 2015 looked at 225 couples with more than three consecutive pregnancy losses compared with 100 control couples with successful pregnancies.  All 225 mothers in the pregnancy loss group carried either compound heterozygous MTHFR C677T and A1298C variants or homozygous C677T or homozygous A1298C. The study defined carrying just one copy (heterozygous) of either C677T or A1298C as being at a low risk for miscarriage.

When the researchers looked at the fathers MTHFR variants, they found that in the pregnancy loss group the men were more likely to carry the risk variants.[study]  This backs up the work of other, smaller studies that also found that the male’s MTHFR status combined with the mother’s MTHFR variants does seem to statistically increase the risk of miscarriage.[study]



How to check your MTHFR variants on 23andMe

Check your 23andMe results for rs1801133 for the MTHFR C677T:

  • GG: normal (wildtype)
  • AG: one copy of C677T allele (heterozygous), MTHFR efficiency reduced by 40%
  • AA: two copies of C677T (homozygous), MTHFR efficiency reduced by 70 – 80%


Check your 23andMe results for rs1801131 for the MTHFR A1298C:

  • TT: normal (wildtype)
  • GT: one copy of A1298C allele (heterozygous), MTHFR efficiency reduced
  • GG: two copies of A1298C (homozygous), MTHFR efficiency reduced




There are a couple of things that could be going on here:
First, fathers who carry the MTHFR variants are likely passing them on to the baby.  There are a couple of studies showing that the baby’s MTHFR variants may play a role in miscarriages, but there are other studies showing no effect from the baby’s MTHFR gene. Overall, the meta-studies tend to show little to no effect from the baby’s MTHFR status, so this is probably not the reason.[study]

The second possibility of why the father’s MTHFR variants matter could tie in with the fact that men carrying homozygous MTHFR variants are also at a higher risk for infertility.  A meta-analysis pooled the results of 20+ studies and showed that men carrying either the homozygous MTHFR C677T or A1298C variants were at a higher risk for infertility (29 – 63% increase).  Statistics here…  Keep in mind that this is the just the increase in the risk of infertility compared to the normal risk. For example, if the risk of male infertility is 1 in 20, a 69% increase would make the risk 1.69 in 20.[study]

Dads matter – in conception, pregnancy, and throughout life! It is easy to see how prospective moms need to clean up their diets, exercise, and sleep well before getting pregnant, but I think these studies are a good reminder that prospective fathers need to pay attention to their own health as well!

MTHFR variants (read more here) increase the need for ensuring adequate folate consumption. This means leafy green veggies, legumes, and other organic food sources of folate need to be eaten daily. If you won’t make the necessary dietary changes, there are methyl folate supplements as well. A quality B12 is also important, and many people find it convenient to take a B-complex to cover all the bases.  Here is one that I like: Jarrow B-Right. But you may find other options that are a better fit for you.

This may be a ‘talk to your doctor’ situation if you have a physician working with you on family planning.  I know – telling some guys to talk to a doctor is like banging your head against the wall, but if recurrent miscarriages or infertility are a problem, this really may be a time to get some professional help.

I didn’t find any specific studies looking at men supplementing with folate for recurrent miscarriage, but there are studies showing that it is effective for women. One recent (small) study found that 5mg of methyl folate along with B6 and B12 decreased the risk of miscarriage.[study]

Please note that methyl folate is likely the better form of supplemental folate vs. folic acid,[study]  but that some studies show that a folate-rich diet is as effective as either methyl folate or folic acid. [study]  One reason for methyl folate instead of folic acid is that there have been several recent studies linking high doses of folic acid to things like an increased risk of allergies[ study] and some epigenetic changes that are a bit of an unknown.[study]

Studies on miscarriage risk for women carrying MTHFR variants:




Review of 23andMe’s GrandTree Feature

Ever wonder whether you get your red hair from your grandmother or grandfather? Is it grandma’s fault that you are likely to go bald?

The GrandTree feature on 23andMe allows you to link together three generations to see what a grandchild inherited from their grandparents. This seems to be the ultimate way to know who to blame for

The GrandTree feature starts off by giving a great explanation of how inheritance works – and why grandchildren don’t necessarily have exactly 25% of their grandparent’s DNA.

Part of the explanation of recombination from 23andMe’s GrandTree


Once you have all everyone sharing their reports with each other, it is easy to go in and select who occupies each branch of the tree.  The Total DNA Inheritance option shows how much DNA each grandchild shares with a grandparent. For example, this ranges, in the case of my kids, between 21 and 31%.

If you have the health reports for everyone included in the sharing, you can also see some fun health and trait sharing information. Highly important information can be gained — such as who to blame for your unibrow genes or from whom your cheek dimples are likely to have come.

None of the traits are highly impactful or vitally important, but it is fun to see how inheritance works in a nice visual format.  One nice feature is to be able to trace a particular gene; if there is one particular gene that interests you, you can trace it back to see which grandparent it came from.


More to Read:

Circadian Rhythm Connections: Part 1 – Mood Disorders

Roosters crowing at the first crack of daylight. Morning glories unfurling their blooms as the sun rises in the sky. Lightning bugs flickering just as dusk falls.

Most people intuitively understand that plants respond to sunlight, using photosynthesis to produce energy and store sugar during daylight.  It is easy to also apply the thought of daily rhythms to animals, with nocturnal mice scurrying around at night and diurnal birds chirping in the morning.

What is often more difficult to understand is how deeply circadian rhythms are hardwired into us, humans. While evolutionary biologist may argue exactly how the circadian clocks evolved through different species, there is no argument that all animals and plants are governed by circadian rhythms, from blue-green algae preparing for sunrise to much more complex organisms with nocturnal and diurnal patterns.[ref]

Why is it so hard for us to understand that humans also are affected by light and dark?

Human hubris?  We are superior, beyond the animal rhythms of nature.  We craft tools for extending light into the night, and our society now functions 24 hours a day. Take back the night. Light it up; party all night.

But it seems that our chickens have come home to roost (pun intended).  This human determination to conquer the night, a 24-hour society of hustling and bustling, is probably at the root of so many diseases including mood disorders, cancers, heart disease, dementia, and diabetes.  In fact, over the course of this multi-part series of articles, I will make the case that research studies are showing that circadian disruption is at the heart of most of our chronic health problems.

Before you mentally check out and decide that this article doesn’t apply to you, I challenge you to read to the end and check out the overwhelming evidence for yourself.

This isn’t hippie-dippie, crackpot, wacko stuff. There is a true abundance of evidence that ignoring our circadian rhythm is fundamentally detrimental to our health.

This goes much deeper than just the standard, oft-repeated advice that you should sleep well. Everyone knows that they should sleep well – and most ignore it.  Sleep is involved, but I think I can make the case that good sleep is a byproduct of good circadian function.

The flow of science usually starts with observing a phenomenon. It is talked about, poked-and-prodded, and theories fly. But a true understanding of a phenomenon or a disease comes with understanding the mechanisms that cause it, reverse-engineering it. One way of reverse-engineering chronic diseases is to look at the genes that cause an increased risk for a disease. Modeling the disease state can then happen in an animal model using genetic manipulation, or knocking out a gene to see the effect.  It isn’t as neat and straightforward in biology as it is in engineering, but the principle remains the same.

My path into investigating the impact of circadian rhythms started with diving into genetics and a fascination with the genes that control our core circadian clocks. Humans (like all animals) have a few core genes that regulate our internal rhythms such as the rise and fall of our hormones, enzymes level fluctuation, cellular repair, body temperature, and the sleep/wake cycle.

Our core circadian rhythm is set by the rising levels of two proteins, CLOCK and BMAL1, that join together each day. Levels of CLOCK and BMAL1 rise over the daylight hours, eventually getting to a high enough level that they inhibit themselves, thus allowing the subsequent increase of the other half of our circadian genes: PER (period) and CRY (cryptochrome).  This feedback loop runs on approximately a 24-hour rhythm.

Notice the word approximately. Circadian comes from the Latin words circa (about) and dia (day). About a day. The daily fluctuations of our circadian rhythms usually take a little over 24 hours for humans kept in total darkness, and other animals may have slightly shorter than 24 hour periods. The CLOCK and BMAL1 timing needs to be regularly set and adjusted.

So what sets the beginning of our daily rhythm: morning sunlight.

The shorter wavelengths of sunlight in the 450-480nm wavelengths, what we perceive as blue light, are exciting a non-image forming photoreceptor in the retina of the eye that signals the beginning of the day. Like a lock and key, the specific wavelength of blue light causes the excitation of the molecule, triggering the signal for our circadian clock. (If you think back to plant biology, this same mechanism is at  work in photosynthesis with a specific wavelength of light exciting the chlorophyll pigment inside the chloroplast.)

If you are thinking back to high school biology and only rods and cones in the retina that form images, you may be surprised to find that there is a third type of photoreceptor in the eye known as intrinsically photosensitive retinal ganglion cells (ipRGC’s). The blue light-sensitive pigment in these cells is known as melanopsin, and it has only been known for less than 20 years.[ref]

So if our eyes are not supposed to be exposed to light at night, what about the fact that we have had light at night ever since our caveman ancestors first lit up a fire to keep their caves toasty at night? Good question. Firelight (and light from candles, oil lamps, etc) gives a nice warm glow; it is mainly light in the yellow and red end of the visible light spectrum without any of the shorter, blue wavelengths.

Over 100 years ago we conquered the night with electric lights, but these incandescent bulbs also cast a warm, yellowish light with only a little in the blue wavelength spectrum. Black and white TV’s came into living rooms in the ‘50’s, and by the 1980’s everyone had color TV’s pouring blue flickering light out into the night as we sat glued to the Duke of Hazard and The A-Team.

Fast forward thirty more years to our current era of ubiquitous devices such as cell phones, tablets, and laptops, all glowing with light in the shorter, blue wavelengths.  Add in the effects of LED and compact fluorescent light bulbs, which both have sharp peaks of blue wavelengths in their spectrum – the pure white light includes a lot of blue light in it. (Anyone else here see the irony of the government banning incandescent light bulb production in favor of the lights that are increasing our chronic health problems?)

We are now bombarding the receptors in our retinas at night with light in the exact wavelength (480nm) that signals to our brain that it is daytime.

All of this core circadian oscillation is taking place in a region of the brain called the suprachiasmatic nucleus (SCN).  Located in the hypothalamus the SCN is connected to the retina and receives the signal from the ipRGC’s. One interesting fact about the SCN is that when it is isolated from the rest of the brain, the cells still maintain electrical and molecular rhythms – the clock keeps on ticking.[ref]

It helps to visualize the rise and fall of the circadian genes like a sine wave, with the amplitude (height) of the wave being important as well as the phase (length of time) affecting us.

Let’s get into some of the scientific studies that investigate the importance of our circadian rhythm.

Mood Disorders:
In 2005, the NIH estimated that 9.5% of the adult population suffered from mood disorders.[ref] The 2016 statistics show that 18.3% of US adults suffer from a mental illness (which is a bit broader of a category than just mood disorder).[ref]  This topic is relevant to so many of us, and the science linking mood disorders to circadian dysfunction leads us to new solutions and alternatives to the psychiatric medications that so often come with side effects.

Seasonal Affective Disorder:
Let’s start with an easy and obvious example:  Seasonal Affective Disorder (SAD) is a well-known disorder that involves the onset of depressive symptoms with the changing amount of daylight in the fall or winter. SAD affects between 2 – 9% of the population, depending on the latitude. It is now thought that the decreased intensity or brightness of the light is what triggers SAD rather than a shorter period of daylight. One effective therapy for seasonal affective disorder is bright light therapy.[ref]  More to read: Genetics of Seasonal Affective Disorder

A study of diurnal (active during daylight) rats found that decreasing the intensity of light could effectively cause anxiety-like behavior. In other words, dim light was causal for mood disturbance. The researchers also found that the decreased light intensity caused a disruption to the HPA axis with increased corticosterone production.[ref]  Corticosterone in rodents is equivalent to cortisol production in humans.

Bipolar disorder:
The link between circadian disruption and bipolar disorder has been known since before the 1970’s. Bipolar patients with a shortened circadian period are the ones who respond to lithium carbonate[ref], which has recently been shown to inhibit GSK3beta, directly impacting the core clock genes. Lithium also causes an increase in the amplitude of the production core circadian protein PER2[ref]

The worldwide lifetime risk of bipolar disorder is a little over 2%, with onset most likely occurring between the ages of 17-27.  One mutation in the gene, CLOCK, causes people to be more likely to stay up a little later in the evenings (evening chronotype); it is also linked to a doubling of the risk of bipolar disease.  [ref]

Major depressive disorder (MDD) has also been linked to circadian disruption. Our neurotransmitter levels of serotonin, norepinephrine, and dopamine all fluctuate with a circadian rhythm over the day. Moreover, MAOA (monoamine oxidase A), which terminates dopamine signaling, is a transcriptional target of the core circadian genes, BMAL1 and PER2.[ref]

It is interesting to look at how antidepressants work. Studies show that SSRI’s shorten or advanced the circadian period, and fluoxetine (Prozac) also causes phase advances.[ref] It is thought that SSRI’s are increasing serotonin in the SCN (suprachiasmatic nucleus), and part of the reason that it takes a little time for them to be effective is that they are changing the body’s circadian rhythm which takes a little while to adjust.[ref]

This brings us back to the chicken or the egg argument. Are mood disorders causing the changes in circadian rhythms or are alter circadian rhythms causing mood disorders?[ref] There seem to be arguments on both sides, and it could be that both sides are correct in that the interrelated feedback loops could keep driving the dysfunction.[ref]

One strong argument for circadian dysfunction causing mood disorders is that genetic variants in the core circadian genes are linked to increased risk of major depressive disorder, bipolar disorder, and anxiety. Another strong link is that altering the CLOCK gene in mice can produce a mouse model of depression. One specific strain, called CLOCKdelta19 mice, causes a longer circadian period with mania and anxiety during daylight and euthymia in darkness[ref] Knockdown of BMAL1 in the SCN of mice induced helplessness, behavioral despair, anxiety and weight gain.[ref]

But not all circadian gene mutations cause mood disorders. Per1 and Per2 mouse mutant strains have altered circadian rhythms without mood alterations. This has led some to hypothesize that light, rather than circadian rhythm, plays a causal role in mood disorders.[ref] While a genetic variant of the CLOCK gene may double the risk of bipolar disorder, obviously not everyone with the variant will become bipolar.[ref]

Looking at animal models of depression adds more fuel to both sides of the argument.  Chronic mild stress causes a dampening in the amplitude of circadian rhythms in mice. It also causes a damping of amplitudes of daily temperature variations and of corticosterone production.[ref]

What do human studies show?
Shift workers who alter their schedules for work are at an increased risk for depression.[ref] While the numbers vary depending on the study, a 2017 meta-analysis came up with a conservative estimate of a 43% increase in the risk of depression for those who work the night shift.[ref]

A number of human core clock genes are associated with the risk for MDD and seasonal affective disorder. Again, finding that circadian gene variants can cause mood disorders is a strong indicator that circadian disruption drives mood disorders.  Recently, it was shown that a PER3 mutation that causes Familial Advanced Sleep Phase Disorder (people who have this naturally want to go to sleep very early in the evening and get up extremely early in the morning) also is causal for seasonal affective disorder. The same study created a mouse model that decreased PER3 expression, which showed that not only were the mice depressed, but the severity of depression was worse with a shorter photoperiod. [ref]

A study of patients with depression looked at the gene expression at the time of death (you can’t do a lot of in vivo studies on gene expression in the brain with people who are living). The study found that compared to non-depressed, people with depression controls who had died at the same time of day showed a phase delay in gene expression, strongly linking circadian rhythm changes to depression.  [ref]

Sleep disturbance goes along with altered circadian rhythms, and sleep disturbances are a hallmark of both bipolar disorder and depression. It is theorized that dampened and shifted circadian rhythms can explain the sleep disturbances in mood disorders. Indeed, dampened temperature fluctuations (our body temperature is supposed to drop at night) and dampened hormonal rhythms are a big part of depression. In bipolar patients, it has been shown that circadian gene expression is phase advanced in manic states and delayed during periods of depression. [ref]

A recent study of blue-blocking glasses for bipolar patients had very positive results.  The study used two groups of patients, one group wearing blue-blocking glasses from 6 pm to 8 am for seven days, while the other group wore clear lenses. After seven days, the group wearing blue-blocking glasses had a drop in the Young Mania Rating Scale of 14.1 compared to the placebo group which had a drop of 1.7.[ref]  Simple, inexpensive, and effective – blocking blue light in the evenings had a significant impact after only a week.

Let me wrap this up by pointing out some things that may seem obvious now:

  • We are a society that is chronically somewhat stressed.
  • Most of us spend the majority of our day inside with low amounts of light (compared to sunlight).
  • We are constantly telling our body that it is morning instead of night by our use of electronic devices with blue light hitting our eyes at night.
  • All of this is having a deleterious effect on our circadian rhythm.


Block the Blue Light at Night:  
Blue-blocking glasses (amber or orange colored lenses) in the evening for a couple of hours before bedtime.  This means wearing them constantly since less than a minute of blue light can delay melatonin onset for quite a while. One study found a 50% increase in melatonin production after just two weeks of wearing blue-blocking glasses. [ref] Be sure to look for ones that block 100% of the blue light wavelengths.

Alternatively, you could stop watching TV in the evenings, avoid reading from a lighted eReader, and refrain from looking at your cell phones, tablets, and laptops. Couple the avoidance of all electronics with low lighting in your house from bulbs that have a red hue and you are on the right track to resetting your circadian clock.

Bright Light During the Day:
Sunlight during the daytime is really important. There is just no way to get enough brightness from normal light bulbs during the day. Try eating your breakfast and lunch outside, or park farther from work and walk in the sunshine for a bit before your day begins. Just make it a priority to get some sunlight. A study shows that even sitting next to a window in your office can help. [ref]  Another study found that increasing morning light decreased depression and increased sleep quality. [ref]

Light therapy devices are becoming more and more prevalent, and the studies on them are showing efficacy for more than just seasonal affective disorder. One recent clinical trial found light therapy effective for postpartum depression [ref], and another in dementia patients also found bright light therapy effective.[ref] There are literally a couple thousand studies available on light therapy for depression, so I would encourage you to research the topic. Note that for most studies on depressed patients, the participants continue their current depression medication during the trial. If you are currently on medication, please don’t just throw out your bottle of pills and turn on a bright light—talk with your doctor and come up with a plan.

Darkness at Night:
Dark Therapy has been tried for some bipolar patients, with forced darkness for 10 hours per night leading to stabilization in mood.[ref] Along those same lines, all of us can benefit from blocking out all light sources in our bedrooms while we sleep. Get some blackout curtains (inexpensive on Amazon), and cover up all the little LED lights on chargers, etc.

Final thoughts:
Read and learn more,  pay attention to your circadian rhythm, and realize that the inconvenience of staying on a normal sleep/wake routine more than pays off in benefits for your long-term mental and physical health.


Are you allergic to grass pollen? It may be genetic.

Spring is in full force here, and with it has come the need to dust off the lawnmower.  As the smell of fresh cut grass fills the air, many people also know the feelings of watery eyes, runny noses, and itching everything.

Speaking of smelling the grass… Did you know that some people can’t smell the odor of fresh cut grass?  There is actually a genetic variant (not covered by 23andMe data) that prevents some people from knowing that wonderful summertime smell.

There are several different gene variants that are tied to an increased risk of grass pollen allergies.

A study found that in people with grass pollen allergies there was an upregulation of MC1R in their noses.  If that gene sounds familiar, it is the same gene that codes for the melanin receptor which causes red hair.

HLA-DRB4 gene:

Human leukocyte antigens (HLA) are part of our immune system and help the body recognize foreign invaders. People have many different variants of these genes, giving rise to protection against different pathogens. Different HLA types lead to an increased ability to fight off diseases and also lead to increased susceptibility to autoimmune diseases and allergies.

rs7775228  (v4, v5)

  • CC: more likely to be allergic to grass pollen[ref]
  • CT: more likely to be allergic to grass pollen
  • TT: normal (most common genotype)

FLG gene:

Filaggrin, a protein encoded by the FLG gene, increases the epithelial integrity. Variants that decrease filaggrin have been tied to different types of allergies.

rs61816761 R501X (v4, v5):

  • AA: (rare) more likely to be allergic to grass pollen [ref]
  • AG: more likely to be allergic to grass pollen
  • GG: normal (most common genotype)

IL2 gene:

Interleukin 2 (IL2) is involved in the body’s immune system response to foreign invaders. It is a cytokine produced by Th1 cells when they are stimulated by, in this case, an allergen.

rs2069762 -330T/G (v4, v5):

  • AA: normal (most common genotype)
  • AG: normal risk of grass allergy
  • GG: 2.6x increased risk of grass allergy, [ref]

IL33 gene:

Interleukin 33 is involved in the body’s immune system response, also.  IL-33 drives the production of Th2 cytokines, acting on mast cells (among others).  It is thought to be responsible for itching sensations from allergies.[ref]

rs928413 (v4, v5)

  • AA: normal
  • AG: increased risk of hay fever, allergy
  • GG: increased risk of hay fever [ref]


A study on children with seasonal pollen allergies compared the effects of 1,000 IU of Vitamin D daily vs. placebo. The study found that the vitamin D group had reduced allergy symptoms compared to the placebo group. Another study looked at vitamin D combined with Lactobacillus rhamnosus GG (probiotic) on children’s allergies and found that the combo was also effective.

Nasal rinsing has been shown to be effective for grass pollen allergies.[ref]  The easiest way to nasal rinse is using a sinus rinse kit or with a neti pot.

Spirulina, a new favorite of mine, has been found in studies to reduce the symptoms of allergic rhinitis.[ref][ref]  You should be able to find spirulina in any health food store, or you can get it online.  Look for an organic version.

Bifidobacterium lactis reduced grass pollen reactions (taken for 8 weeks). [ref]

If you normally take antihistamines for pollen allergies, this study suggests that taking the antihistamines for three days before the exposure prevented the histamine 1 (H1) receptors from increasing expression in the nose. In an allergic response, your body releases histamine as a signaling molecule and then the receptors for histamine cause the reaction to occur.  H1 receptors are the ones involved in your typical seasonal allergy reaction with a runny nose and itchy, watery eyes. So the study showed that without the increase in histamine receptors, there were few allergy type symptoms. The antihistamine prevented the body from upregulating the H1 receptors.

Lithium: A mineral that affects mood, Alzheimer’s disease, obesity, and telomeres

I’ve written before on the topic of supplemental lithium orotate for mood, anxiety, and irritability. (Read the previous article here: A little lithium and B12 makes the world a happier place — for some.)

What about the effects of lithium as a mineral supplement on other aspects of health?

In reading studies on a wide range of other topics over the past three years, several links to lithium have popped up. Topics such as circadian rhythm dysfunction, Alzheimer’s disease, telomere length, type 2 diabetes, and obesity… not the subjects that I expected to lead me back to lithium!

The rest of this article lays out the evidence that increasingly shows the importance of this mineral in our health and longevity. I think it is important to examine the research and look at the long-term effects and safety questions that always come to mind when talking about lithium. There is such a stigma, at least in my mind, around lithium that I’ve hesitated at times to talk with friends and family about it – a hesitation that no one seems to have in recommending other minerals such as magnesium or potassium.

Lithium orotate supplements compared to prescription lithium carbonate:
I want to clarify before getting into the studies on lithium what ranges of dosages the studies are talking about. The prescription medication that most people are familiar with for bipolar disorder is usually in the form of lithium carbonate.

Standard doses of lithium carbonate are around 900-1200mg/day, although this can vary based on the individual. For lithium carbonate, there is about 18.8 mg of elemental lithium per 100mg of lithium carbonate. So a 900mg dose would give about 170mg elemental lithium.[ref]

Lithium orotate usually comes as a 120mg supplement that gives about 5mg of elemental lithium.

The amount of lithium that we get in foods and drinking water varies based on the mineral content of the soil, with estimates of .5 to 3mg per day. A provisional RDA of 1mg/day has been recommended. [ref]  So a 120mg lithium orotate (5mg elemental lithium) supplement would average around twice the normal daily consumption from food and water, while the prescription dosages are closer to 80 to 100 times normal daily intake.

Alzheimer’s Disease:
A new study came out in November 2017 on Alzheimer’s rates and natural lithium levels in the drinking water in Texas. In an article about the study (which is easier to read than the research paper:-), the lead author of the study explains the findings. Water samples from almost all of the counties in Texas were tested for their natural levels of the mineral lithium, which varies depending on the concentration in rock and soil.

The researchers found that Texas counties with higher levels of lithium in their groundwater had less of an increase in Alzheimer’s rates compared with counties that had lower levels of lithium. This isn’t a total surprise since previous studies had linked lithium to a decreased risk of dementia, but it is a great confirmation at a large scale population level.  A lot of the initial studies were observations linking bipolar patients taking large doses of lithium carbonate and having lower rates of dementia.

A sampling of other recent studies on lithium and Alzheimer’s disease:

  • A 2015 review in the Journal of Alzheimer’s Disease analyzed the data from three randomized placebo-controlled clinical trials of lithium for treating patients who had already been diagnosed with Alzheimer’s disease. The trials found that lithium “significantly decreased cognitive decline as compared to placebo”.
  • An October 2017 article in JAMA Psychiatry details a nationwide study in Denmark on the exposure to lithium in drinking water and the incidences of dementia.  This was a large study, with 73,000+ dementia patients and 733,000+ people without dementia as the control. The study found that there was a decreased rate of dementia in those people exposed to naturally higher levels of lithium in their water (measured since 1986).
  • A March 2018 animal study looked into the mechanisms of how lithium chloride lowers the risk of Alzheimer’s. It found that lithium chloride caused an increase in soluble β-amyloid clearance from the brain. In mice genetically bred to be a model of human Alzheimer’s, lithium chloride restored the clearance of soluble β-amyloid to the levels of normal mice. One big thing to note from this study is that lithium chloride did not affect β-amyloid that had formed plaque already.
  • A study in 2015 looked at the effects of microdoses of lithium on a mouse model of Alzheimer’s disease. The study found that small doses of lithium carbonate in the drinking water of mice carrying the genes for Alzheimer’s disease caused “decreased number of senile plaques, no neuronal loss in cortex and hippocampus and increased BDNF density in cortex, when compared to non-treated transgenic mice.” This was a follow-up study to the human study in 2013 which showed that microdoses of lithium stopped the cognitive decline in Alzheimer’s patients.

You may be wondering at this point why all doctors aren’t handing out low doses of lithium to everyone at risk for Alzheimer’s. I think the quick answer is that it isn’t the ‘standard of care’ with enough clinical trials backing it up. The cynical side of me also notes that lithium orotate (and aspartate) are cheap, over-the-counter supplements without pharmaceutical companies sponsoring huge trials and pushing doctors to prescribe them. There seems to be a couple of ‘novel’ low-dose formulations in the works by pharmaceutical companies, though. [ref][ref][ref]

Telomeres and aging:
Telomeres are the sequences of DNA that are found at the ends of each chromosome. This sequence protects the ends of the chromosome from deterioration. The common example given is to think of telomeres like the plastic on the end of shoelaces that protects the shoelace from fraying. When cells undergo cellular reproduction (mitosis), a little bit of the telomere is lost, and thus telomere length is considered a biomarker of cellular aging. Shorter telomere length is associated with several age-related chronic diseases including Alzheimer’s.

A recent transgenic mouse study found that lithium carbonate treatment leads to longer telomere length in mice that are bred to have Alzheimer’s disease. Interestingly, the normal mice had no effect on telomere length from lithium.  A meta-analysis of 13 studies found that Alzheimer’s patients have shorter telomeres.

A human study looked at telomere length in patients with bipolar disorder. The study found that patients with bipolar disorder (not on lithium) and their relatives had shorter telomeres lengths than healthy, unrelated people. More interestingly, patients with bipolar disorder who were lithium-treated had longer telomere length than patients with bipolar disorder who were not taking lithium as well as relatives of bipolar patients.

Telomere length is a new field of investigation for researchers looking into so many different topics of aging, longevity, and disease. I don’t think the handful of studies on telomere lengthening from lithium really lead to a conclusion yet; I look forward to seeing what future studies tell us on the topic.

Anti-Inflammatory action of lithium:
Lithium exerts some anti-inflammatory effects on the body as well as pro-inflammatory effects under some conditions. It has been known since the 1970’s that lithium inhibits prostaglandin synthesis and COX2 in some parts of the brain. While there is some debate on the topic, the majority of studies also point to lithium decreasing the production of TNF-α, a pro-inflammatory cytokine.[ref]

A recent cell study looked at the potential of lithium plus caffeine, theobromine, and catechin on the innate immune system and inflammation.  The results showed that stacking lithium with caffeine, theobromine, and catechin was more effective as an anti-inflammatory than using them separately.

Another recent study looked at the anti-inflammatory effects of lithium on cells containing the SOD2 genetic variant rs4880.  The study found that those with rs4880 alanine allele (GG for 23andMe) had more of an anti-inflammatory response than those with the valine allele (AA for 23andMe).  This was a cell study though, so it is hard to know how well this translates to the whole body.

Obesity and Type 2 Diabetes:
What surprised me about the Nov. 2017 study that I referenced above was that Texas counties with higher levels of lithium in their water also had lower levels of obesity and diabetes.  I was surprised by this because one of the side effects of long-term, high dose lithium carbonate usage is an increased risk of hypothyroidism and possible weight gain.

Part of the explanation for the high levels of lithium in water correlating to lower levels of obesity and diabetes may be due to the effects on circadian rhythm. Another possible connection between lithium, obesity, and T2D may be the effect on blood glucose levels. In mice, certain levels of lithium reduced non-fasting blood glucose levels.[ref]

How is lithium affecting our body and brain?
For a long time, it wasn’t really understood how lithium worked for bipolar patients. (Quite a few psychiatric medications have been used for decades without fully understanding the mechanisms by which they work – or don’t work – for people.) Studies over the past decade or two have shed light on the neurobiological mechanisms of lithium and genetic studies have increased that knowledge.

One effect of chronic, low-dose lithium is an increase in BDNF, which is a protein that promotes the growth of nerve cells.[ref]

The American Chemical Society published a great overview the topic in 2014, “Neuroprotective Effects of Lithium: Implications for the Treatment of Alzheimer’s Disease and Related Neurodegenerative Disorders“. One of the effects of lithium is its inhibition of GSK-3β (glycogen synthase kinase-3 beta), which is involved in neuronal cell development and energy metabolism. Genetic mutations of GSK-3β increase the risk of bipolar disease.

Lithium ions compete with sodium and magnesium ions in the body for binding sites in certain circumstances. Lithium’s inhibitory effect on GSK-3β is thought to be due, in part, to binding to a site that is normally occupied by magnesium. For a very thorough overview of the biochemical properties of lithium, including its effect on the activation energy of water within a cell and its effect on mitochondrial function, please read through “Towards a Unified Understanding of Lithium Action in Basic Biology and its Significance for Applied Biology“.

One action of GSK-3β is its inhibition of glycogen synthase, which is an enzyme involved in the reaction that takes excess glucose and turns it into glycogen for storage. Thus inhibiting GSK-3β increases glycogen synthesis and increases insulin sensitivity.[ref][ref]

GSK-3β and Circadian Rhythm:
Our body’s core circadian clock is run by a couple of core genes that are expressed during the day and a couple of core circadian genes that rise at night. It is this daily rise and fall of gene expression that then drives our internal daily cycles of waking and sleeping, temperature, and energy metabolism. GSK-3β is involved in phosphorylation of both the day and night core circadian genes.

Genetic variants that change our circadian rhythm are linked to increased risk for bipolar disorder. People with bipolar disorder who respond well to lithium therapy have changes in their circadian gene expression when they take lithium.[ref][ref][ref][ref]

Prevention of lead toxicity:
A recent article hypothesized that some of the benefits reported for higher lithium levels in the drinking water (lower suicide rate, lower homicide and crime rates) could be due to lithium mitigating the effects of lead toxicity. “Animal studies demonstrated that lithium pre-treatment mitigates lead toxicity.”

Toxicity of lithium:
Lithium is considered by some to be an essential trace element, and a complete elimination of lithium causes a decline in fertility, higher mortality rates, and behavioral abnormalities.[ref] But, like all substances, there is always a toxic upper limit.

Patients taking lithium carbonate or lithium chloride for mood stabilization show a variety of side effects, depending on dosing. Most patients taking prescription lithium carbonate get blood tests done at regular intervals to determine their serum lithium levels. Plasma lithium levels above 1.2 mM cause nausea, diarrhea, and tremor. [ref]  Other side effects noted by patients taking lithium chloride include increased thirst and urination, weight gain, and mental dullness. It was theorized that bipolar patients taking lithium may drink more calories due to increased thirst, thus causing weight gain.[ref] Other side-effects of higher doses of lithium include increased risk of kidney problems and interaction with hypothyroidism.

Lithium orotate, as a supplement, comes in much, much lower doses than the lithium in prescription lithium carbonate. There is one case report, though, of nausea and mild tremor from a teenager taking 18 tablets of a supplement that contained 100mg of lithium orotate.

Side effects of Lithium Orotate:
There aren’t any recent research studies or case reports (other than the one above) on lithium orotate side effects, so this section is n=1 personal experiences and internet hearsay. A couple of people that I’ve talked with have reported that lithium may make them tired or a little sleepy during the day, but this was pretty subjective and could have been due to other reasons. An article from a holistic doctor who suggests lithium orotate to most of his patients notes that very few have any side effects. He does suggest taking lithium orotate before bed instead of during the day. This makes sense in light of the circadian rhythm effects via GSK-3B inhibition. A study from 1986 on using lithium orotate for alcoholism listed minor side effects to the treatment (included more than just lithium orotate -e.g. low carb diet and other supplements) as loss of appetite, mild apathy, and muscle weakness. [ref]


If after reading through all the information about lithium orotate you want to add it to your supplement list, here are a couple of brands that are well regarded by my family: Weyland’s Lithium Orotate and Seeking Health Lithium Orotate.

As with any supplement, I suggest talking with your doctor if you are on medication or if pregnant or nursing.

The study on stacking lithium with caffeine, theobromine, and catechin for an increased anti-inflammatory effect was interesting. If you are considering this combo, a good source of theobromine is cacao nibs.  Catechins and caffeine are found in green tea.




Gulf War Illness: Genetic susceptibility and current research

A question from a patron via Patreon prompted me to look into the link between genes and Gulf War Illness. I wanted to share what I found in case it can help other veterans who are dealing with the aftereffects of their service to our country during the Gulf War.

The Dept. of Veteran Affairs explains that they don’t use the term Gulf War Syndrome or Gulf War Illness because of the variety of the medically unexplained symptoms. For simplicity here, I will use the term Gulf War Illness (GWI) because ‘chronic multisymptom illness that is medically unexplained’ is way too long and vague. The VA does state that it “presumes certain chronic, unexplained symptoms existing for 6 months or more are related to Gulf War service without regard to cause.” It includes quite of list of illnesses including chronic fatigue syndrome, fibromyalgia, functional gastrointestinal disorders (IBS, dyspepsia, and abdominal pain), and undiagnosed illnesses (“abnormal weight loss, fatigue, cardiovascular disease, muscle and joint pain, headache, menstrual disorders, neurological and psychological problems, skin conditions, respiratory disorders, and sleep disturbances.“). That is quite an eye-opening list of the depth and breadth of the problems faced by Gulf War veterans! [ref]

It is estimated that 250,000 – 300,000 of the US veterans that served in the Gulf War have GWI, and veterans from the UK were also affected. There were approximately 700,000 US troops involved in the Gulf War, so about 1/3 are affected in some way by chronic illnesses. [ref] [ref]

There have been multiple theories proposed for the causal agent for GWI. Some of these theories include exposure to an infectious disease, exposure to biological or chemical weapons, vaccinations, depleted uranium exposure, and exposure to a variety of different chemical agents including pyridostigmine bromide, organophosphate pesticides, decontamination agents, and petroleum exposure due to both fumes and oil well fire smoke. [ref]

As you can see, military personnel were exposed to multiple environmental toxins. It is entirely likely that there is not just one single cause of GWI, and exposure to one toxin could have lead to increased susceptibility to another environmental agent.

A 2008 government report that combined information from more than 100 different studies points the finger towards pyridostigmine bromide, pesticides, and possible exposure to low levels of sarin nerve-gas. You can read the full 465-page report.

I always find it interesting to look at how researchers create mouse or rat models of illnesses for their studies. For Gulf War Illness, researchers give mice pyridostigmine bromide (PB), DEET, and permethrin (a pyrethroid insecticide), and then they stress the rats out for a period of time. [ref]  PB is a medication that was given as a preventative for sarin nerve gas exposure.  DEET and permethrin were insecticides that were used by military personnel.

The link between PB, pesticides, and sarin gas is that all of these affect the body’s central nervous system through their effect on choline esterases. DEET not only affects the olfactory system of insects (mosquitoes dislike the smell of it), but it also inhibits cholinesterase activity in humans and strengthens the toxicity of another type of pesticides, carbamates. [ref] Permethrin is commonly used on clothing and mosquito netting to kill insects, and it is also used to kill lice.

So how is genetics involved in all of this? Genes play a huge role in how our bodies react to environmental toxins. Some people are better than others at detoxifying different substance, including medications and toxins. (I have a whole bunch of articles on genetic variants involved in detoxification if you want more information on the topic.)

Genetic Variants Studied for Gulf War Illness

BChE genetic variants:
Butyrylcholinesterase is an enzyme coded for by the BCHE gene. It is mainly produced in the liver and found in the blood plasma. A deficiency in BChE can be caused by a couple of variants of the gene. BChE deficiency causes the body not to metabolize several different compounds as quickly as it should. Compounds metabolized by BChE include cocaine, heroin, and several anesthetics/nerve blocking drugs (succinylcholine, mivacurium, and procaine). Additionally, BChE prevents organophosphate nerve agents (including sarin gas) and organophosphate insecticides from affecting the nervous system. People with genetic variants causing a decrease in the body’s production of BChE have a higher risk of being affected by organophosphates and of having adverse reactions to the anesthesia’s listed above.[ref]

Pyridostigmine bromine, which is an acetylcholinesterase inhibitor, was taken as a protective measure against nerve agents by about half of our military personnel in the Gulf War. One study found that personnel who took PB and were within a mile of an exploding SCUD missile (a stressor) were about 3 times more likely to have GWI. Veterans who had been in support areas who used personal pesticides also had an increased risk (12x) of GWI. [ref]

PB, as well as other acetylcholinesterase inhibitors, interact with both BChE and acetylcholinesterase (AChE). BChE is present in the blood at 10x the amount of AChE, and it protects people from having adverse reactions to carbamates and organophosphates (insecticides). [ref] (Note that there are virtually no AChE genetic variants affecting enzyme activity because it would cause embryonic lethality.[ref])

One fairly common genetic variant that reduces BChE levels by 14-30% is the rs1803274 T allele. This is known in studies as the K variant. One study of GWI links it (along with other less active BChE variants) to up to a 40x increased risk of GWI. This is a huge increase in the risk! [ref]

Check your 23andMe results for rs1803274 (v.4, v.5):

  • TT: K variant, ~14% reduction in BChE, increased risk of GWI [ref]
  • CT: carrier of one copy of the K variant, reduced BChE, increased risk of GWI
  • CC: normal

Another variant, found in about 1% of the population of the BChE gene is rs1799807. It is called the ‘atypical’ version of BChE in studies and has only about 40% of normal enzyme activity. [ref]  If you have the atypical variant, you should tell your doctor this before having surgery, since it affects recovery from anesthetics.

Check your 23andMe results for rs1799807 (v4, v5 and also AncestryDNA):

  • TT: normal
  • CT: ‘atypical’ version of BChE, increased risk of GWI
  • CC: ‘atypical’ version of BChE, greatly increased risk of GWI

Additionally, there are 20+ other mutations (all rare) that result in significantly decreased BChE enzyme. These aren’t all covered in 23andMe data. [ref]

PON1 genetic variants:
Human susceptibility to adverse effects from organochloride pesticides (permethrin is one) is modified by the PON1 gene. The PON1 gene codes for paraoxonase, which is an enzyme that breaks down a number of different organophosphorus compounds such as nerve gas and insecticides. It also is the enzyme that protects LDL cholesterol from oxidation (oxidized cholesterol is thought to be the cause of atherosclerosis, hardening of the arteries).

A very common genetic variant in PON1 is rs662. The ‘Q’ allele, which corresponds to the T genotype, is associated with lower PON1 activity and a higher risk of GWI. (Note that the TT genotype for rs662 is very common with almost half of Caucasians carrying it.) [ref ][ref]

Recent studies have also found that this PON1 variant increases the risk of cardiovascular disease, due to PON1’s effect on HDL levels, especially in people exposed to pesticides (e.g. coffee harvesters, sheep farmers). [ref] [ref] It is also linked to increased risk of anxiety and depression in those exposed to organophosphorus pesticides.

The research on the PON1 rs662 variant is extensive in looking at its effect on cardiovascular disease – extensive and contradictory. The effects of the variant seem to be related to ethnicity and also to environmental exposures. Not only does current exposure to pesticides have an effect, but also prenatal pesticide exposure changes the DNA methylation patterns of the gene (epigenetically decreasing the function of it). So while you can look at your genetics here, also keep in mind that your mom’s exposure to pesticides before your birth may play a role as well. [ref][ref]

Check your 23andMe results for rs662 (v.4, v.5):

  • TT: possibly higher risk of GWI[ref]
  • CC: normal risk of GWI

Another study on PON1 levels in Gulf War veterans found that the average PON1 activity was lower in all Gulf War veterans regardless of genotype when compared to Bosnian peacekeeping veterans or nondeployed military personnel. [ref]

HLA DRB*13:02 Genetic Variant, Autoimmunity, and Inflammation:
Some veterans are protected from brain atrophy in GWI, depending on whether they carry a specific HLA type. [ref] [ref] This may explain part of the differences in severity of symptoms.

So what is an HLA type? The HLA (human leukocyte antigen) system is part of our adaptive immune system, the part of our immune system that remembers previous exposure to pathogens or toxins. For example, the adaptive immune system is what ‘remembers’ that you have already had the chicken pox and then can very quickly attack and destroy the virus if you are exposed again.

More specifically, HLA  is a really complex system that brings parts of a molecule to the surface of a cell to signal that the cell needs to be destroyed by the body’s killer T-cells. Back to the example of the chicken pox virus – if a cell gets re-infected by the virus, the HLA system brings a piece of the virus to the surface of the cell, signaling for the immune system to destroy the whole cell and thus destroying the virus that is replicating inside of the cell. There are a bunch of different HLA types with a variety of different components that bring about a huge number of possible combination to counteract foreign invaders of all types. People inherit different alleles of the different HLA types, and because this system is highly polymorphic, susceptibility varies to different types of invaders or to autoimmune disease. Overall, for the human species, this is really important to survival so that no single disease wipes us all out.

There have been a couple of studies showing that veterans who carry one particular HLA type, HLA DRB1*13:02, are less likely to have brain atrophy due to Gulf War Illness. In looking at genetic data, rs4759997 is linked to having HLA DRB1*13:02. [ref] This rs number is not contained in either 23andMe or Ancestry data at this time.

So why include this information here if the rs id isn’t included in common sources of genetic data? The mechanism by which the HLA DRB1*13:02 allele is protective is probably through its ability to eliminate some of the antigens that are causing chronic, low-grade inflammation and possibly autoimmunity.

The link to an autoimmune component in Gulf War Illness is important because many autoimmune conditions can be helped through diet.

Beyond the HLA DRB1*13:02 link to autoimmunity, there are other studies that indicate a possible immune system involvement in GWI. One (small) study found that veterans with GW had greater levels of inflammatory cytokines (IL-1B and IL-15) on days with higher fatigue severity. [ref] A larger study found that several different inflammatory proteins were elevated in veterans with GWI.[ref]

A final link to the immune system response can be found in a recent study using a rat model of GWI (PB, pesticides, and 4 weeks of stress). The study found that quite a few genes related to oxidative stress, antioxidant activity, neuroinflammation, and mitochondrial respiration were all upregulated, which means that all of those systems were activated in response to the chemicals and stress. This study concludes: “These results imply that chronic oxidative stress, inflammation, and mitochondrial dysfunction in the hippocampus, and heightened systemic inflammation and oxidative stress likely underlie the persistent memory and mood dysfunction observed in GWI.” [ref]


I don’t think there is a magic pill (yet?) to cure Gulf War Illness. The supplements and diet recommendations below may provide some help in healing your body. The best bet may actually be to try all of them.

Curcumin: A study commisioned by the Dept. of Defense used rats that were exposed to low doses of GWI-related chemicals to test the effects of curcumin supplements. The study found enhanced neurogenesis (growth of neurons in the brain) and decreased inflammation in the brain. The study also found that oxidative stress was reduced and mitochondrial function was increased, all thought to increase mood and memory. [ref]

Curcumin is a natural substance found in turmeric, which is a spice used in making curries. Turmeric is not all that well absorbed by the body on its own, so there have been curcumin supplements developed that contain piperine, which increases the body’s ability to absorb and use curcumin. Here are a couple of options: BioSchwartz Curcumin and Jarrow Curcumin. There are other good brands as well, and you can probably find curcumin at your local grocery store.

CoQ10: Tying into the effects discussed above on mitochondrial function, CoQ10 has been shown in a randomized control trial to help with GWI symptoms. The study, which ran for 3.5 months, found a 100mg dose to work the best.[ref]  CoQ10 is a well studied and readily available supplement.  If you are interested in other ways to improve mitochondrial function, you may want to read Dave Asprey’s book Head Strong.

Sleep: A study on improving sleep quality found that it was effective in reducing depression and fatigue symptoms in Gulf War veterans. [ref] Mind-body bridging, which I hadn’t ever heard of before, is what they used in the study to improve sleep quality.[ref] Another research backed method of improving sleep quality includes blocking blue light at night by wearing blue-blocking glasses for two hours before bed. (This is one ‘lifehack’ that works really well for me!)

Diet: Considering the possible autoimmune link, check into what is known as the Autoimmune Protocol diet. Here is a good article on it:  There is no real downside to trying this diet, and several people that I know with autoimmune diseases swear by it.

Avoid DEET, permethrin, and insecticides in general. Nope, I don’t have a study on this specifically for GWI, but it is common sense that if exposure to these insecticides was part of the problem then avoiding further exposure is probably warranted.

There are a few alternatives to DEET, such as picaridin and lemon eucalyptus. Especially avoid DEET combined with other insecticides that are carbamates. [ref]

Permethrin is a very commonly used pesticide. If you have a company coming out to treat your home for bugs each year, you should check to see what kind of chemicals they are spraying. In agriculture, it is mostly used on wheat, corn, and cotton. Consider going with organic foods and possibly organic cotton. [ref]  I was surprised to find out how extremely common it is to have permethrin in the body.  A new study came out recently showing that it was found in 90% of breast milk samples.[ref]

Stress: Another way to create a rat model of GWI is to expose them to 4 days of corticosterone (equivalent to the effect of cortisol in humans) before injecting with a sarin nerve agent surrogate. High cortisol levels can be caused by chronic stress. It is conjecture on my part, but lowering cortisol levels (if they are high) may also help with some of the symptoms of GWI. Yoga, mindfulness meditation, or ashwagandha root supplement may help lower your cortisol levels. [ref]

Along that same line of thought, a 2016 study of Gulf War veterans found that mindfulness-based stress reduction reduces pain, fatigue, and cognitive failures. [ref] There are lots of websites and videos on mindfulness, and there are several good phone apps as well.

Acupuncture: A Dept. of Defense sponsored study looked at the effectiveness of acupuncture as a treatment for GWI. It found that acupuncture reduced pain and reduced physical disability. [ref]

NRF2 activators: One more suggestion (that isn’t based on any GWI specific research) is to look at supplements that increase NRF2. Rat models of GWI showed that the NRF2 pathway was involved. In general, NRF2 is involved in the body’s antioxidant defense system; it activates glutathione S-transferase and NQO1. Curcumin boosts NRF2, as does sulforaphane from broccoli sprouts.[ref]

Research to keep an eye on:
Reversing the neuronal effects: A study from July 2017 looked at the effects of GWI on human neurons. It found that there were problems with microtubule acetylation, and they were able to reverse it with an HDAC6 inhibitor. So in a basic sense, some of the genes in the neurons are turned off in GWI, and with the HDAC6 inhibitor, they re able to return the genes to normal function. This is somewhat hopeful if researchers can use it in the brain rather than just in a petri dish. HDAC6 inhibitors are in human clinical trials now for cancer and a few other diseases. [ref]

Light therapy: Another research avenue to investigate is the use of transcranial red/near-infrared LED light therapy. There are studies going on with GWI veterans for this type of treatment.[ref] If you are interested in investigating it, you may also want to search for photobiomodulation in addition to low-level laser therapy.

What didn’t work:
Doxycycline: A large VA trial of doxycycline for possible mycotoxin-related illness did not show any benefits. [ref]

Mifepristone, a corticosteroid, didn’t show much of an effect on GWI although it did boost visual learning a little.[ref]

Carnosine: A clinical trial of carnosine also showed little effect other than a possible effect on memory. “12 weeks of carnosine (1500 mg) may have beneficial cognitive effects in GWI. Fatigue, pain, hyperalgesia, activity and other outcomes were resistant to treatment.”[ref]

Final thought:

I want to thank all of our Gulf War veterans for their service to our country, and I hope that the information provided here will be a good starting point for finding relief from their symptoms. Please keep in mind that I’m not a doctor, and everything here is just my summary of research studies on the topic. I am sure that I have left some (probably important) things out, and I’m hopeful that there is much more research coming out soon on the topic.

How to download your AncestryDNA raw data and import it into Excel

A quick tutorial for today on downloading your data from AncestryDNA.

Why download your data?  Well, it is YOUR data — genetic data about you that you paid for…  If you download it from AncestryDNA, then you can use that data in a variety of ways. You also don’t have to worry about the company going out of business or cutting off access to the download file.

Step 1) Log in to

Step 2) Go to your Settings

Step 3) Click the Download Raw DNA Data button.

Step 4)  Read, check the acknowledgment box, and then enter your password again.

Step 5) Wait for an email from AncestryDNA with a link to download the file.

Step 6) Click the link in the email from AncestryDNA.  It will take you to the page to download your data.

Step 7) Your DNA Raw Data file will download as a .zip file to your default downloads directory. For most computers, you can just double-click to unzip the file.   I suggest saving it to another folder and also to an external or backup drive so that you don’t lose the file.

Optional:  Import the file into Excel

While you can unzip your raw DNA data file and look at it using a text editor (Notepad, TextEdit, etc), I find it easiest to import it into Excel for searching and keeping notes on what I’ve learned about a particular gene.

Before you ask…  no, you cannot import it into Google Sheets. The file has too many rows. 

There are several ways to import a text file into Excel, so if the directions below don’t quite match up with your version of Excel, you can always do a quick Google search for alternatives.

Step 1) Open up a new workbook and select the Data tab.  Click on the From Text icon.

Step 2) Select your raw DNA data file. (It is probably named AncestryDNA.txt.) Then you will see the data import wizard.

Step 3) The next couple of screens in the Text Import Wizard should all have the right default values already chose for your tab-delimited text file. You will just need to hit “Next” and then “Finish”.  You can put the data into your existing blank worksheet.

Step 4)  It may take a minute for the text file to be imported.  It is almost 700,000 rows of data.  Be patient. Don’t mess with Excel while it is importing.

Step 5) Now you can search your data using the Find command in Excel.  Go ahead and give it a try.  Look for rs4988235.  If your results show a G and a G for your genotype, you are likely lactose intolerant (or not producing lactase) as an adult.  Read the Lactose Intolerance article for all the details.

I suggest setting up a second sheet in the Excel workbook and using it to take notes on what you learn about your genetics. Then start looking through this blog to figure out other things you would like to know:


Don’t forget to save your Excel file in a safe place :-)

5 ways you can optimize your diet today, based on your genes

With all the dietary advice out there today, how can you know what is right for your body?

I’ve boiled down 5 quick ways that you can use your genetic data (23andMe, AncestryDNA, etc) to optimize your diet to fit your genes.

#1) Are you genetically lactose intolerant?

Lactase is the enzyme that breaks down the sugar, lactose, that is found in milk products.

While most people of European Caucasian ancestry produce lactase as an adult, about 10% of that population doesn’t produce lactase. For people of other ancestries, the majority do not produce lactase as adults.

Check your 23andMe results for rs4988235 (v.4, v.5 of 23andMe; AncestryDNA):
AA: Still produces lactase as an adult
AG: Still produces lactase as an adult (less than those with AA – study)
GG: No longer produces lactase as an adult
Lifehack: If you don’t produce lactase as an adult, you are relying on your gut microbiome to break down the lactose in milk. Drinking less milk at one time, switching to lactose-free milk, or boosting your gut microbiome with some lactose-digesting probiotics are all options for those without the ability to produce lactase.
Read more about the genetics of lactose intolerance.

#2) Are fruits and vegetables giving you enough vitamin A?

Beta-carotene, which makes carrots and sweet potatoes orange, is often considered to be a great source of vitamin A. But some people are much better at converting beta-carotene into vitamin A than others.
A deficiency in vitamin A can cause skin issues (dry scaly skin, acne, keratosis pilaris, cracked lips) and eye issues (dry eyes, problems with night vision).
There are two main genetic variants to check in the BCMO1 gene to see how well you convert beta-carotene.
Check your 23andMe results for rs7501331 (v.4 and v.5):
CC: normal
CT: decreased beta-carotene conversion
TT: decreased beta-carotene conversion
Check your 23andMe results for rs12934922 (v.4 and v.5):
AA: normal
AT: decreased beta-carotene conversion
TT: decreased beta-carotene conversion
Lifehacks: If you have a “T” in both of the SNP’s above, your beta-carotene conversion is almost 70% less than normal.  A “T” in just one SNP from above decreases your conversion by about 32%.[study] Eating liver is a great way to get the retinol form of vitamin A that your body needs.  Can’t stomach liver? A vitamin A supplement that includes retinol palmitate may work for you.
You don’t want to go too far overboard with supplementing with vitamin A since it does get stored by the body.  Read more about vitamin A and your genes.

#3) Is saturated fat increasing your risk of high blood pressure?

A recent study looked at the influence of a higher fat diet (mainly from saturated fat) on blood pressure. The study found that the higher saturated fat diet caused higher blood pressure only in those with a genetic variant known as ACE deletion.

Check your 23andMe results for rs4343 (v4, v5):

  • AA: ACE insertion/insertion
  • AG: ACE deletion/insertion
  • GG: ACE deletion/deletion – saturated fat intake may increase blood pressure

Lifehacks: This is definitely a case where if you have the ACE deletion and higher blood pressure, you should experiment with reducing saturated fat and see if your blood pressure comes down. The study showed approx. a 10 point average difference in systolic blood pressure for those with the ACE deletion and high-fat diet.

Read more about the interaction between high-fat diet, blood pressure, and your genes.

#4) Will drinking coffee in the morning decrease your risk of heart attack?

Coffee is the number one source of antioxidants in the US diet.  Our ability to metabolize the caffeine in coffee varies quite a bit according to our genes.  About half of Caucasian populations are fast metabolizers of coffee, with the other half being slower metabolizers.
Studies have linked coffee consumption to an increased or decreased risk of heart attacks — depending on your caffeine metabolism genes.[study]

Check your 23andMe results for rs762551 (v4, v5):

  •  CC: Slow metabolizer of caffeine, increased risk of heart attack with more than 2-3 cups of coffee per day
  •  AC: Slow metabolizer of caffeine, increased risk of heart attack with more than 2-3 cups of coffee per day
  •  AA: Fast metabolizer of caffeine, decreased risk of heart attack with 2 – 3 cups of coffee a day
 Lifehacks: Common sense dictates if you have a family history of heart disease and slow caffeine metabolism genes, you should consider keeping your coffee consumption at 2 or fewer cups of coffee on an average daily basis.  Alternatively, if you are a fast metabolizer of caffeine you can reduce the risk of heart attack with 3 cups of coffee a day.  The study also showed that for those younger than age 59 who were fast metabolizers of caffeine, drinking 4+ cups a day also decreased the risk of heart attack.

Looking for a way to pep up your morning coffee?  Here are a couple of options:

#5) What about carbs???

A study came out recently showing that both low carb and low-fat diets were equally effective for weight loss. There are other studies showing differences in dieting results of low carb or low fat that depend in part on genetic variants. Looking at your genes may give you an idea of which diet would work best for you.

Amylase is the enzyme that digests of carbs, starting in your mouth.  A genetic variant in the amylase gene (AMY1-AMY2) predicts whether you are likely to produce a lot of the enzyme or less of the enzyme to break down carbs.

Check your 23andMe results for rs11185098 (v.4 only):

  • AA: higher amylase activity
  • AG: intermediate amylase activity
  • GG: lower amylase activity

Your genes also play a role in how carbohydrates are likely to affect your blood glucose levels.

Check your 23andMe results for rs2943641 (v4, v5) IRS1 gene:

  • TT: women had lower T2D risk with low-carb, men had lower T2D risk with lower fat diet[study]
  • CT: women had lower T2D risk with low-carb, men had lower T2D risk with lower fat diet
  • CC: better results with high carb diet (weight loss, insulin)[study]

Check your 23andMe results for rs1800849 (v4) UPC3 gene:

  • AA: no decrease in glucose or insulin levels on high protein/low carb diet [study]
  • AG: no decrease in glucose or insulin levels on high protein/low carb diet
  • GG: lower glucose levels, better weight loss on high protein/low carb diet

Lifehacks: If you are a lower amylase producer but want to try a higher carb / lower fat diet, you can supplement with the amylase enzyme. I recommend actually testing your blood glucose levels to see how you react to different foods/meals.  Blood glucose testing kits are not all that expensive and will give you a way to quantify and keep track of your response.

Read more about amylase genes and carb metabolism and blood glucose genes.

Final Thoughts…

I hope you have found something here that is useful. Personally, I’m often frustrated by the one-size-fits-all approach that so many health and wellness websites proclaim. While I didn’t have huge health problems, the little diet adjustments based on my genes have made a noticeable difference for me. For example, figuring out that I don’t convert beta-carotene to vitamin A lead me to try a supplement of the retinol form of vitamin A.  A month later I noticed that I didn’t have the little bumps (keratosis pilaris) on the back of my arms that had been there since childhood. (And yes, I did test it out to make sure it was the vitamin A by stopping the supplement for a month, at which point the bumps came back.)  While getting rid of bumpy skin isn’t earthshattering, all the little tweaks to my diet and lifestyle based on what I’ve learned from my genes have added up to me being healthier and mentally sharper.