This is: thriftygene.net
I have posted on the gestational diabetes forum (diabetes.co.uk). "All women with the "hunter" gene get gestational diabetes. The symptoms of the "hunter" gene are your glucose tolerance test is slowing down but is still rising for 2 hours. You do not lose weight on a low carb diet. Your A1c is correlated with your diet. Are there any other women who get gestational diabetes?" I received over 2700 hits. The only respondent to my question was 1 women who takes steroids for an organ transplant.
Insulin is used to make cells able to absorb sugar and change it into fat. Insulin is also used to process protein and create urea.
Insulin resistance refers to the fact that even if insulin is in the blood it does not make cells able to absorb sugar and change it into fat. The placenta creates hormones which create total or near total insulin resistance.
My basic premise is that all humans can produce these hormones or similar ones elsewhere in the body and do so when it is obviously advantageous.
Body of Text
Thrifty gene is a theory proposed in 1962 that said since some populations when they switched from their standard diet to the modern diet became fat and often became diabetic they must have a gene that is good when food is scarce but bad when it is plentiful.
Prediabetic was originally defined as too high a blood sugar reading 2 hours after drinking sugar after a fast.
My glucose tolerance test in 1964 (GTT) was originally 70 after ½ hour 130 after 1 hour 175 after 2 hours 185 (extended) after 3 hours 100.
I have read that up to 1/3 the energy available is lost in storing sugar as fat and then changing fat into sugar (correct me if you have better figures).
During 1957 in approximately 2 months I lost approximately 20-25 pounds and developed an overactive bladder and starting to have my fatigue symptom.
I eat a very low sugar/starch diet. Another patient with my form of reactive hypoglycemia says he/she feels fine with a diet which includes slowly absorbing starch.
Warning: People with the other type of reactive hypoglycemia should eat slowly digesting starches and be careful about eating protein (see Atkins tab). If anyone knows a diet which completely or nearly completely prevents low sugar episodes. Tell me about it. I suspect that such a diet would be useful to type 1 diabetics if for some reason they do not take insulin.
My latest readings fasting blood sugar 96 A1c 5.5
Dr Vaidya pointed out that the body produces (Human Placental Lactogen (HPL)) in the placenta while the women is pregnant. These hormones produce insulin resistance. This could be the hormones used to create insulin resistance in the “hunter” gene population.
For me, judging by my GTT my body probably stops the (HPL?) when my blood sugar gets to approximately 170. The time lag before it then tries to mop up the sugar in my blood seems to be over 1 hour.
I had one blood sugar reading when I was feeling sick and tired. My reading was 60.
Recently it was found that an alteration of the MRAP2 gene in mice has lead to an unexplained weight gain. This could be a "hunter" gene in mice.
I have posted on the gestation Forum for diabetes.co.uk. The responses indicate that almost all women who get gestational diabetes have the "hunter" gene. For a fuller explanation go to the tab "Hunter gene + Diet" on the top of this page.
This is an explanation of why I had such disturbing symptoms for about 50 years until I figured out that a very low sugar/starch/alcohol (SSA) diet seemed to be relieving my symptoms. It then took approximately an additional 2 years for almost all my symptoms to clear. It then took about 6 years and a lot of serendipity to figure out what was the problem and that turned out to be only a start of a journey. I am sorry that this explanation is long, but I have been told it is complicated.
It is a fact that about half the women in India have my gene, and it leads to all the sugar problems in pregnancy. Considering my gene, leads to a diagnosis of prediabetes that is what people from India told me. "see A1C tab above" I quote from one nurse who said about the sugar problems in pregnancy “it must be genetic”. "see Hunter gene+Diet tab above"
A major reason for this study is that a doctor on PBS in 2015 drew two graphs of a GTT. GTT’s run for 2 hours. "see Atkins tab above"
The first GTT went up and then down. He indicated this is the expected GTT. The second GTT slowed its rate of assent but was still rising as he lifted his marker. The second is my GTT (2) taken in 1964. Does anyone know the name of this doctor? He defined such people as having a “hunter” gene. He said people with this GTT did not lose weight on his weight loss diet. The diabetic community says this sounds like the “thrifty” gene. I note that the details are different but…. Since people with the “hunter” gene should be better able to survive famines there must be a downside to this gene. I guess one downside is that women with this gene have problems controlling their blood sugar during pregnancy.
The following paragraph contains my actionable conclusions. Details describing them and what lead up to some of these conclusions follow.
Probably my most important conclusion is that Type 2 diabetes could be due to hormones used to create insulin resistance being produced all the time. Researchers, where are you?
In my wildest dreams this article would eventually lead to everyone getting a baseline glucose tolerance test (GTT). I strongly suggest you ask your physician to take a GTT to find out if you have the normal (GTT) or the “hunter” (GTT).
Another dream is that doctors would publicize that you can get an autoimmune disease if you have the “hunter” gene. If you have the “hunter” gene and become chronically fatigued I suggest you see if cutting back your sugar/starch/alcohol (SSA) improves how you feel.
Judging from what people with reactive hypoglycemia post, I have a dream that doctors will realize that what is necessary to avoid all the symptoms of either form of reactive hypoglycemia is to not let the blood sugar go above an unknown value. This value can be completely different for different people. I further guess that both types of reactive hypoglycemia are due to the same autoimmune problem.
From my posts on diabetes.co.uk I conclude that the treatment for reactive hypoglycemia in the U.S. and U.K. are different. The difference comes down to, is the hunter gather diet good for humans? Do we need grains and significant fruits for a healthy diet? My personal experience indicates that a lot of small balanced meals is impractical. You are on the knife edge of going into reactive hypoglycemia.
An even bigger dream is that a very low sugar/starch/alcohol (SSA) diet would be tried on most type 2 diabetics and it successfully controlled high blood sugar; for some diabetics this may be a better option then the standard treatment. In that case make sure you monitor your blood sugar to see if you have cut your sugar/starch/alcohol (SSA) enough.
Another dream is that it would be found that people with the “hunter” gene tend to become fat on the modern diet; for me a low fat diet worked. If you have the “hunter” gene see if this works for you. As the weight loss doctor said, “people with the hunter gene do not lose weight on his weight loss diet”. This would then lead to the following obvious question. Is the hunter gene the reason for the weight problems, when they try the modern diet, with the Indian population, American Indians, Pacific Islanders etc.…? If so, all my advice follows for these people.
I was interrupted by a man from India while I sprouted my theories by “half the people of India are prediabetic (1), but they do not get diabetes”.
This indicates why.
I also present a theory about an alternate method of sugar storage used by some humans. I have the following question: assume a women has sugar problems during pregnancy. How can you see if her GTT has returned to normal after pregnancy if you don’t know what is her normal GTT? I have the following observation: if women with the “hunter” gene are much more susceptible to sugar problems during pregnancy, maybe you can explore possible pre pregnancy interventions with these women.
In 1964 a doctor looked at my GTT and said I was prediabetic (1) and was developing insulin resistance. I am fat and have done all the wrong things, but I am not a diabetic. The reason for my GTT in 1964 is that I get very low blood sugar hours after eating too much SSA. I know of 4 other people with the hunter gene who also have this symptom. I guess that one of the emergency procedures the body uses when the blood sugar gets too low is to start the hormones which create insulin resistance. I also assume this happens before the liver releases sugar. We also have other symptoms starting with much lower values of SSA. The symptoms are some significant degree of brain fog and fatigue. These symptoms are controlled by never letting our blood sugar go above some (unknown) value.
I theorize that the hunter gene allows people to only store sugar when their blood sugar rises above some value (3). Consider the following. Evolutionary changes are often additions to existing processes. Women with the “hunter” gene have insulin resistance in pregnancy. Insulin is needed to process protein. Look at my glucose tolerance test (2). I am led to the following weird conclusion. With the “hunter” gene people are normally in a state of insulin resistance. They are usually simulating a severe type 2 diabetic. When their body determines that the blood sugar is heading for dangerous territory, that it will affect the general chemistry of the blood, the body cuts insulin resistance and if necessary produces insulin to keep the blood sugar from going too high. It waits over an hour in this mode and then produces enough insulin to mop up the excess sugar in the blood.
My wild guess is that the “hunter” or “thrifty” gene people are constantly producing hormones to create insulin resistance (7). When the blood sugar gets too large, they stop producing these hormones and if necessary produce a little insulin, even though they are somewhat insulin resistant. After a time gap to allow the hormones to clear, they produce a large enough quantity of insulin to make most of the sugar in their blood become fat. Sometime into this insulin release they are supposed to restart the hormones. People with reactive hypoglycemia do not restart the hormones. I speculate that people who eat only a moderate amount of (SSA) do not wait the necessary time to clear the hormones as their body determines it is not necessary. They do not get very low blood sugar since they are somewhat insulin resistant. In this case they get fatigue due to not turning on the hormones which produce insulin resistance. The fatigue comes due to mild low blood sugar (8) for extended periods of time and/or from trying to start the hormones. I guess that the enumerable instances when I nearly simultaneously had a very mild shaking and felt better was when my body restarted the hormones which create insulin resistance. I further speculate that people with the “normal” sugar processing also use these hormones for a short time when hypoglycemia threatens. I think that people with either of the reactive hypoglycemia symptoms have disabled this response.
I am on a very low (SSA) diet. I am simulating a severe type 2 diabetic almost all the time. I speculate this was true for the hunters from which I arose.
I have reason to believe that I had an episode which was an autoimmune reaction (4). I therefore theorize that doctors should be aware that it is possible for people to have one type of cell of their adrenal glands destroyed. This compromises the possibly complicated chemistry that allows sugar to be stored based on their blood sugar in “hunter” gene people. Doctors should advise people with the reactive hypoglycemia and GTT that they will feel better if they carefully control the (SSA) in their diet (5). I only know of 5 people with the “hunter” gene autoimmune problem I describe and only two have had their symptoms diagnosed by doctors. The doctors noted that diet controlled their problem but had no idea what was happening. I therefore suggest that doctors make people with the "hunter" gene aware of this possibility.
My diet is low enough in (SSA) that with my "hunter" gene I have turned off the effects of insulin. My evidence is that my fasting blood sugar has risen, but it is very normal, because I never lower it with insulin (6). Further, on occasion, I have gained weight on this diet. I noticed that years ago I was able to lose about 80 pounds in approximately 1 year on a crash diet of pasta with cottage cheese with enough vegetables for vitamins. I also notice that I am presently losing weight on my very low (SSA) diet by cutting out almost all cheese. Since my meat portions are comparatively small, I assume I am losing weight for the standard reason. Further, I have no discernible problem with exercise even with my extreme diet with very low (SSA). My fasting blood sugar remains at near the highest but normal values, ever (6). Have I returned to my hunter roots?
Defined as too high a blood glucose reading 2 hours after ingesting sugar after a fast.
GTT 70, ½ hr 130, 1 hr 175, 2 hr 185, extended 3 hr 100.
I have read that up to 1/3 of the energy in sugar is used up in storing and later releasing the sugar.
During 1957 in approximately 2 months I lost approximately 20-25 pounds developed an overactive bladder and started my fatigue symptom.
I eat a very low sugar/starch diet. Another patient posts, he/she feels fine with a diet which includes slowly absorbing starch.
Latest: Fasting blood sugar 96 A1c 5.5
Dr. Vaidya pointed out that the body produces Human Placental Lactogen (HPL) in pregnancy which creates insulin resistance. This could be the hormones used to create insulin resistance in the “hunter” gene population. Judging by my GTT my body probably stops the (HPL?) when the blood sugar gets to approximately 170. The time lag before it then tries to mop up the sugar in the blood seems to be over 1 hour.
I had one blood sugar reading because I was feeling sick tired it was 60.
*Science, Scientific American and the American Medical Association will not allow me to put my add into their publications. Does anyone have a suggestion on how to over come this problem.
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I wish to give thanks to Dr. Vaidya of Harvard University who has been emailing with me for years as I developed these theories.
I have the "hunter" ("thrifty") gene do you?
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