Autoimmune Thyroid Disease

An Unfortunate and Lengthy Adventure in Misdiagnosis

Monoamine oxidase activity and insulin

with 3 comments

FACT 1: Use of monoamine oxidase inhibitors (MAOIs) are associated with significant weight gain:

Antidepressants such as tricyclic antidepressants and monoamine oxidase (MAO) inhibitors are most often associated with significant weight gain. Pharmacodynamics of drug-induced weight gain.

FACT 2: Common low activity monoamine oxidase single nucleotide polymorphisms are associated with increased weight and increased risk of obesity:

We investigated the association between the monoamine oxidase A (MAO-A) gene and obesity. […] The TDT analysis of the EcoRV polymorphism showed in obese subjects with a body mass index (BMI) >/=35 kg/m(2) a preferential transmission of the low activity-related allele (chi(2)(TDT) = 8.0, p = 0.005). Our findings may provide evidence of a candidate gene involved in obese subjects with a BMI >/=35 kg/m(2). Family-based association study between the monoamine oxidase A gene and obesity: implications for psychopharmacogenetic studies.

We found, however, that both MAOA and MAOB show an excess of the low-activity genotypes in obese individuals. Additionally, the MAOA genotype was significantly associated with both weight and BMI. Obesity is associated with genetic variants that alter dopamine availability.

FACT 3: Monoamine oxidase activity is disturbed in diabetes:

MAO activity in pancreatic tissue is significantly reduced in diabetes. This decrease in MAO activity is associated with an increase in pancreatic tissue levels of adrenaline (ADR) and noradrenaline (NA). Studies on the level of 5-hydroxyindoleacetic acid of pancreatic tissues suggest that serotonin level is also increased in diabetics. Many studies show that MAO inhibits insulin secretion. However, some of its substrates including, serotonin, adrenaline and noradrenaline have been shown to stimulate insulin secretion. In conclusion, the activity and subcellular localisation of MAO suggests that MAO may play an important role in pancreatic beta cell function and hence in the pathogenesis of diabetes mellitus. The effect of diabetes mellitus on the morphology and physiology of monoamine oxidase in the pancreas.

In other words, high MAO activity inhibits insulin secretion. A number of monoamines (serotonin, adrenaline, noradrenaline etc) themselves stimulate insulin secretion, therefore low monoamine oxidase activity automatically leads to higher insulin levels.

FACT 4: Glucose regulates monoamine oxidase activity:

Islet beta-cell monoamines are known to influence the insulin-releasing mechanisms. These amines are localized in the insulin-secretory granules and are inactivated by the enzyme monoamine oxidase (MAO), a hydrogen peroxide (H2O2)-generating enzyme. The activity of islet MAO may consequently be of importance for insulin secretion. In the present investigation, we studied the relation between islet MAO activity and plasma levels of insulin and glucose in obese (ob/ob) hyperglycemic mice and their lean littermates. In addition, the effect of glucose on the MAO activity of in vitro-cultured islets was studied. MAO activity was assayed with serotonin, dopamine (DA), and beta-phenylethylamine (PEA) as substrates. After an overnight fast in adult (age, 6 months) lean mice, islet MAO activity was increased by 35% to 70%. Plasma levels of glucose and insulin were markedly decreased as expected. However, fasting in adult obese mice either did not affect islet MAO activity (PEA and DA) or induced a slight decrease (serotonin) of approximately 25% (P < .05). Plasma glucose levels in adult obese mice were not significantly affected by the overnight fast. However, a correlation analysis based on individual adult obese mice (fed and fasted) showed a negative correlation between plasma glucose concentration and islet MAO activity with PEA (r = -.65, P < .02) and DA (r = -.66, P < .02), respectively. Further, a positive correlation (r = +.58, P < .05) was found between glucose level and islet MAO activity when using serotonin as substrate. There was no difference in islet MAO activity with PEA and DA as substrates in fed obese versus fed lean mice. Glucose modulation of islet monoamine oxidase activity in lean and obese hyperglycemic mice.

In other words, lowering blood glucose through fasting caused monoamine oxidase activity to increase dramatically. In obese mice, blood glucose remained high and monoamine oxidase activity did not increase.

My own blood glucose levels are consistently on the edge of high-normal, even on a low-carb diet, and if they got any higher I would actually be classified as a T2 diabetic.

This explains to me why low carbohydrate diets and intermittent fasting have helped myself and a number of people I know who are sensitive to food chemicals. Even regular low calorie diets seem to help some people. I’ve often noted that the consumption of amine containing foods has the ability to cause massive, sudden weight gain in myself. I’ve also noted that when I am on a ketogenic diet I have a higher tolerance of amines.

It also explains something else. I’ve met a lot of people who really, really believe that low carbohydrate diets are THE answer to everything, and these people have been overweight for years and nothing worked except low carbing. Often they describe symptoms that correlate with food chemical sensitivity. What these people do not know is that they are overweight because they have low monoamine oxidase activity.

I imagine that when you combine low monoamine oxidase activity with other polymorphisms that increase insulin or insulin-like growth factor output (like the vitamin D receptor polymorphism VDR Fok), you have a recipe for reactive hypoglycaemia, weight gain and diabetes. Another reason for me to suspect I have both of these polymorphisms.

So now it seems that ALL failsafe food chemicals raise insulin levels – glutamates, salicylates, and amines.

I’ll spell this out again for the sake of the low-carbers whose eyes glaze over: the reason obesity is an increasing problem these days is not just due to increased consumption of carbohydrate. It is also due to the grossly increased amounts of food flavour chemicals eaten in the modern Western diet.


Written by alienrobotgirl

13 January, 2008 at 6:00 pm

Posted in The Genetics of FCI?

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3 Responses

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  1. You are very clever and i have read your complete blog. I have several problems with chemicals, and i have lost all my intelligence because of the chemicals which makes me ill, fatigue, depressive, etc. I have lost my job too because i could not handle my problems and a job, i was always SICK and felt like DYING slowly, sadly i never died, but i hoped to because my life was not a life anymore. So through your genius intelligence you have helped me a lot and i make great improvements.


    14 January, 2008 at 11:45 pm

  2. I can vouch for this from my own personal experience. Amine-y foods make me gain weight, too, even at ZERO carbs.

    Mother Nuture

    15 January, 2008 at 4:05 pm

  3. Hi anonymous – I hope you’re feeling better on failsafe. Wow. You read the whole of my blog? That’s impressive!

    Alien Robot Girl

    30 January, 2008 at 1:25 pm

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