Low Vitamin D and Diabetes

Researchers measured Vitamin D levels in over 5,000 people without diabetes. After five years, researchers measured Vitamin D levels again and determined that 200 of the participants had developed diabetes. They found that 6 in 100 people with low Vitamin D levels developed diabetes, versus 3 in 100 with regular levels that developed diabetes. When they factored in diabetes risk factors, the risk of diabetes increased to 57%.

Is Sugar Toxic? Does fructose contribute to obesity and diabetes?

Feed animals enough pure fructose or enough sugar, and their livers convert the fructose into fat — the saturated fatty acid, palmitate, to be precise, that supposedly gives us heart disease when we eat it, by raising LDL cholesterol. The fat accumulates in the liver, and insulin resistance and metabolic syndrome follow.

Michael Pagliassotti, a Colorado State University biochemist who did many of the relevant animal studies in the late 1990s, says these changes can happen in as little as a week if the animals are fed sugar or fructose in huge amounts — 60 or 70 percent of the calories in their diets. They can take several months if the animals are fed something closer to what humans (in America) actually consume — around 20 percent of the calories in their diet. Stop feeding them the sugar, in either case, and the fatty liver promptly goes away, and with it the insulin resistance.

When Tappy fed his human subjects the equivalent of the fructose in 8 to 10 cans of Coke or Pepsi a day — a “pretty high dose,” he says —– their livers would start to become insulin-resistant, and their triglycerides would go up in just a few days. 

Thompson believes that many pre-cancerous cells would never acquire the mutations that turn them into malignant tumors if they weren’t being driven by insulin to take up more and more blood sugar and metabolize it.

To me this suggests that fructose at least plays SOME role in metabolic syndrome

Pesticides are linked to multiple problems : Parkinson's, diabetes & lung cancer.

http://www.safelawns.org/blog/index.php/2011/05/researchers-find-link-between-third-pesticide-and-parkinsons-disease/

IN 2009, researchers at UCLA linked Parkinson’s Disease (PD) to two chemicals commonly sprayed on crops to fight pests. The study didn’t examine farmers, but rather focused on people living near the farm fields where the chemicals maneb and paraquat were sprayed. They found that, for those residents, the risk for PD increased 75%.

A follow-up study adds two new twists. Funded by the National Institutes of Environmental Health Sciences and Neurological Disorders and Stroke, the U.S. Department of Defense Prostate Cancer Research Program, and the American Parkinson’s Disease Association, researchers have now implicated a third pesticide, ziram.

This time, the population tested also included people who worked near sprayed fields- including firefighters, teachers, and clerks. They found that the combined exposure to ziram, maneb and paraquat near any workplace increased the risk of PD threefold, while combined exposure to ziram and paraquat alone was associated with an 80 percent increase in risk. The results appear in the current online edition of the European Journal of Epidemiology.

http://www.neurology.org/content/50/5/1346.abstract

When adjusted for these variables and smoking status, there was a significant association of occupational exposure to herbicides (odds ratio [OR], 4.10; 95% CI, 1.37, 12.24) and insecticides (OR, 3.55; 95% CI, 1.75, 7.18) with PD, but no relation was found with fungicide exposure. Farming as an occupation was significantly associated with PD (OR, 2.79; 95% CI, 1.03, 7.55), but there was no increased risk of the disease with rural or farm residence or well water use

Both insecticides and herbicides — most notably organochlorines, organophosphorus compounds, chlorophenoxy acids/esters, and botanicals — significantly increased the risk of Parkinson’s disease, the researchers report in the online journal BioMedCentral (BMC) Neurology.

http://aje.oxfordjournals.org/content/167/10/1235

Using logistic regression, the authors considered two primary measures of pesticide exposure: ever use and cumulative lifetime days of use. They found seven specific pesticides (aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor, and cyanazine) for which the odds of diabetes incidence increased with both ever use and cumulative days of use. Applicators who had used the organochlorine insecticides aldrin, chlordane, and heptachlor more than 100 lifetime days had 51%, 63%, and 94% increased odds of diabetes, respectively

http://newswise.com/articles/view/541427/

http://www.latimes.com/health/boostershots/la-heb-pesticides-parkinsons-20110526,0,4772737.story

California researchers who first established a link between two commonly used pesticides and Parkinson’s disease have found a third crop-enhancing chemical — ziram — that appears to raise the risk of developing the movement disorder.And they have found that people whose workplaces were close to fields sprayed with these chemicals — not just those who live nearby — are at higher risk of developing Parkinson’s.

In animal studies conducted as part of the research on agricultural chemicals and Parkinson’s disease, the researchers found that ziram was powerfully destructive to neurons that use the transmitter chemical dopamine to send messages. These brain cells are the ones that die off in regions of the brain that govern motor function, causing the tremors, unsteady gait and difficulty initiating movement that are the hallmarks of Parkinson’s.

http://peer.ccsd.cnrs.fr/docs/00/57/38/99/PDF/PEER_stage2_10.1080%252F02652030903031171.pdf
When compared to applicators who had never used these chemicals, those who had used metolachlor over 457 lifetime days had a four-fold risk of lung cancer. For those who had usedpendimethalin more than 225 days, their risk was 3.5 times greater for developing lung cancer.

Too much fructose leads to weight gain & diabetes. Don't gorge on fruit.

fructose is “isocaloric but not isometabolic.” This means you can have the identical amount of calories from fructose or glucose, fructose and protein, or fructose and fat, but the metabolic effect will be entirely different.

fructose consumption leads to decreased signaling to the central nervous system from two hormones, leptin and insulin, both of which play key roles in hunger and satiety, as well as weight control.

Here’s a linked paper which gives a bit more science

Because fructose does not stimulate insulin secretion from pancreatic ß cells, the consumption of foods and beverages containing fructose produces smaller postprandial insulin excursions than does consumption of glucose-containing carbohydrate. Because leptin production is regulated by insulin responses to meals, fructose consumption also reduces circulating leptin concentrations. The combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae. In addition, fructose, compared with glucose, is preferentially metabolized to lipid in the liver. Fructose consumption induces insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriacylglycerolemia, and hypertension in animal models.

high-carbohydrate meals stimulate leptin production in humans relative to high-fat meals

Diets high in fructose induce insulin resistance in rodents (87–89) and in dogs (90). For example, Thorburn et al (91) fed rats a diet containing 35% of energy as fructose for 4 wk and found reduced insulin sensitivity associated with impaired hepatic insulin action and whole-body glucose disposal. 

There are numerous studies in which dietary fructose has been shown to induce hyperlipidemia in rodents (104, 107–109). Herman et al (107) reported that rats fed a high-fructose diet had sustained elevations in serum triacylglycerol. Circulating triacylglycerol concentrations rose and remained elevated during the entire time fructose was fed (100 d) and fell promptly when a standard chow diet was instituted. The same investigators also concluded that there was a greater capacity of human liver to metabolize fructose to lipid compared with glucose because high-sucrose diets led to elevated serum triacylglycerol concentrations in humans, whereas the same amount of glucose resulted in lower concentrations of serum triacylglycerol 

Similar to insulin resistance and hyperlipidemia, many published experiments have shown that high-fructose diets induce hypertension in animals, including rodents (125–128) and dogs (90).

To put it in simpler terms…when you eat fructose alone, your blood sugar levels remain elevated. Not only that, but your liver tends to convert the fructose into fat, so the amount of in your blood gets elevated.  Not only that, but you don’t get the same feeling of fullness, so you just tend to eat more. If your there is too much fat in your bloodstream, you eventually get diabetes.

Here is an article that talks about that

a defect in insulin-stimulated glucose transport in skeletal muscle is the primary metabolic abnormality in insulin-resistant type 2 diabetics. Fatty acids appear to cause this defect in glucose transport by inhibiting insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-1 associated phosphatidylinositol 3-kinase activity.

Here is a table, listing the amount of fructose present in various foods

Fruit Serving Size Grams of Fructose

Limes 1 medium 0

Lemons 1 medium 0.6

Cranberries 1 cup 0.7

Passion fruit 1 medium 0.9

Prune 1 medium 1.2

Apricot 1 medium 1.3

Guava 2 medium 2.2

Date (Deglet Noor style) 1 medium 2.6

Cantaloupe 1/8 of med. melon 2.8

Raspberries 1 cup 3.0

Clementine 1 medium 3.4

Kiwifruit 1 medium 3.4

Blackberries 1 cup 3.5

Star fruit 1 medium 3.6

Cherries, sweet 10 3.8

Strawberries 1 cup 3.8

Cherries, sour 1 cup 4.0

Pineapple 1 slice

(3.5” x .75”) 4.0

Grapefruit, pink or red 1/2 medium 4.3

Boysenberries 1 cup 4.6

Tangerine/mandarin orange 1 medium 4.8

Nectarine 1 medium 5.4

Peach 1 medium 5.9

Orange (navel) 1 medium 6.1

Papaya 1/2 medium 6.3

Honeydew 1/8 of med. melon 6.7

Banana 1 medium 7.1

Blueberries 1 cup 7.4

Date (Medjool) 1 medium 7.7

Apple (composite) 1 medium 9.5

Persimmon 1 medium 10.6

Watermelon 1/16 med. melon 11.3

Pear 1 medium 11.8

Raisins 1/4 cup 12.3

Grapes, seedless (green or red) 1 cup 12.4

Mango 1/2 medium 16.2

Apricots, dried 1 cup 16.4

Figs, dried 1 cup 23.0

It’s worth noting that this table is somewhat skewed. 1/16 of a water melon is 286 grams, where as a medium orange is less than half that. Who’s to say you won’t eat 1/32 of a watermelon etc.

This site, listing fructose amounts per 100g is also useful.

Agave / Agave nectar - Has a high fructose-to-glucose ratio

Aparagus  - Contains significant amounts of fructans

Apples - 6g fructose per 100g

Artichoke  - Contains significant amounts of fructans

Banana - 4.85g fructose per 100g

Blackberries - 2.4g fructose per 100g

Blueberries - 5.0g fructose per 100g

Cherries - 5.3g fructose per 100g

Currants - 3.5g fructose per 100g

Grapes - 8g fructose per 100g

Honeydew Melon - 2.9g fructose per 100g

Inulin  - Source of fructans; sometimes added to foods such as yoghurt

Kiwi fruit - 4.3g fructose per 100g

Lemon Lime soda/softdrink - 5.8g fructose per 100g

Mango - 5.5g fructose per 100g

Onion  - Contains significant amounts of fructans

Orange juice - 2.7g fructose per 100g

Oranges - 2.2g fructose per 100g

Pears - 6.2g fructose per 100g

Pineapple - 7.2g fructose per 100g

Plum - 3.0g fructose per 100g

Raisins - 30g fructose per 100g

Raspberries - 2.3g fructose per 100g

Strawberries - 2.4g fructose per 100g

Tangerines - 2.4g fructose per 100g

Watermelon - 3.35g fructose per 100g

Note that agave syrup is blamed because of its high fructose to glucose ratio, which is ironic because it’s claimed as a healthy alternative, and arguably healthier choices could be found.

Fructans is mentioned above

A fructan is a polymer of fructose molecules. They occur in foods such as agave, artichokes, asparagus, green beans, leeks, onions (including spring onions), yacon, jícama, and wheat.

Some people have trouble digesting fructose, and for those with intestinal difficulties, it is recommended that they avoid fructans.

Here’s some more about fructose malabsorption syndrome

Even in healthy persons, however, only about 25-50g of fructose per sitting can be properly absorbed. Persons with fructose malabsorption may absorb less than 25g per sitting.

This is yet another reason not to have too much fructose at once.

The article also has this table, which is interesting

Food Fructose (grams / 100 grams) Glucose (grams / 100 grams)

Sucrose (for reference) 50 50

Apples 5.9 2.4

Pears 6.2 2.8

Fruit juice e.g. Apples, Pears 5 to 7 2 to 3

Watermelon 3.4 1.6

Raisins 29.8 27.8

Honey 40.9 35.7

High fructose corn syrup 42 to 55 45 to 58

It’s not that the ratio is particularly worse in high fructose corn syrup - it’s that the quantity of sugar consumed is typically much larger than that that would be consumed when eating fruit.

If you eat small enough portions, less sugar enters your system and therefore less insulin is needed to control a blood sugar rise, and therefore less damage is done.

Let’s look at how many calories are actually burned from eating and sitting around.

A person who weighs 150 lbs. burns about 64 calories per hour while sleeping; someone who weighs 200 lbs. burns approximately 86 calories per hour while sleeping, according to Fit Watch.

Eating burns about 140 calories per hour; watching TV or reading burns around 75; and doing homework, or anything that requires heavy concentration or brain activity, burns around 110.

Let’s be generous and assume 100 calories per hour are burned. That’s 25 grams of carbohydrate. So if you were taking small nibbles or a few pieces of fruit here and there, that’s about 1.5 pieces oranges per hour, about 200 grams of orange. The calculations are similar for standard serving sizes of other fruits. Assuming there is some glucose in the fruit, for which there will be an insulin response, the amount you can eat rises somewhat.

How to make sense of the data on fructose? As I see it, each food has a functional purpose. Protein sources like steak are effective at building muscles. On the other hand if early man came upon an orchard full of fruit in the early summer, he might well gorge and it might be an evolutionary advantage for him to get fatter to take advantage of all the fruit in front of him. Now, as fruit is available in huge quantities everywhere, the possibility of getting fat from gorging on fruit is real. 

What’s the upshot? If you want to lose weight and attain better health, pay attention to the amount of fructose you consume.

If you want to improve your insulin response, consider combining fruit with protein, as protein causes insulin levels to rise, without affecting your blood sugar.

Pure protein — protein sources that do not contain any carbohydrates — do not affect your blood glucose levels

Insulin does many things at once. It causes amino acids to be taken in to cells and causes blood sugar to be lowered via a number of different mechanisms.

So, as I see it the takeaways are:

1) Avoid sugary drinks and any drinks with high fructose corn syrups (includes most sodas).

2) If you are eating a fruit that contains fructose, don’t eat too much, so as not to raise the blood sugar too high, as insulin won’t help enough. Don’t gorge on fruit. 

3) Consider eating fruit with a meal in which you have some protein.

4) Be careful with respect to the total amount of fructose you consume in any given day. The less fructose you consume the better it is for your blood sugar & the more it prevents obesity, but fruit is good for other reasons, so try to find the compromise that’s right for you.

Megapost : First Gluten was identified. Now comes lectins, found in wheat, grains, rice, potatoes etc. Lectins can impair digestive health, mental health, cardiovascular health, and cellular function. Lectins can contribute to weight gain and diabetes, and can impair your immune system.

I continue to be interested in paleolithic diet theory. We’ve only been eating milk and grains for 10,000 years, and it takes considerably longer than that to adapt to new food groups. So it is therefore likely that we do not have the right biological structures in place to deal with those foods. As time goes by research increasingly supports this conclusion. We know that certain proteins in dairy products are linked with heart disease and poor circulation. We know that gluten can cause a plethora of problems even in those who test negative for celiac. We’re just beginning to scratch the surface when it comes to other components in other grains and dairy.

First let’s go over WGA, or wheat germ agglutinin, and the issues it brings up.

Lectin is a defense mechanism for the wheat plant, designed to ward of its natural enemies such as fungi and insects. Unfortunately, this protein is also very resistant to breakdown by living systems, and it easily accumulates in tissues where it interferes with normal biological processes and acts as an anti-nutrient.

  • Pro-Inflammatory: WGA lectin stimulates the synthesis of pro-inflammatory chemical messangers, even at very small concentrations.

  • Immunotoxic: WGA lectin may bind to and activate white blood cells.

  • Neurotoxic: WGA lectin can pass through your blood-brain barrier and may attach to the protective coating on your nerves known as the myelin sheath. It is also capable of inhibiting nerve growth factor, which is important for the growth, maintenance, and survival of certain target neurons.

  • Cytotoxic (Toxic to cells): WGA lectin may induce programmed cell death.

Further, research shows WGA lectin may even:

  • Interfere with gene expression

  • Disrupt endocrine function

  • Adversely affect gastrointestinal function

WGA lectin is capable of passing through cell membranes of your intestines, gaining entry into your body. Further, if your mucosal barrier is compromised, for instance from taking certain drugs like aspirin and ibuprofen or due to a viral or bacterial infection, lectin may become even more problematic.

Keep in mind that lectin is not only in wheat. All seeds of the grass family (rice, wheat, spelt, rye, etc.) have high levels of lectin.

Here’s more:

WGA lectin is an exceptionally tough adversary as it is formed by the same disulfide bonds that make vulcanized rubber and human hair so strong, flexible and durable. Like man-made pesticides, lectins are extremely small, resistant to break-down by living systems, and tend to accumulate and become incorporated into tissues where they interfere with normal biological processes. Indeed, WGA lectin is so powerful as an insecticide that biotech firms have used recombinant DNA technology to create genetically modified WGA-enhanced plants. 

Lectins are glycoproteins, and through thousands of years of selectively breeding wheat for increasingly larger quantities of protein, the concentration of WGA lectin has increased proportionately.

Lectins are designed “to choose” specific carbohydrates that project off the surface of cells and upon which they attach. In the case of WGA the two glycoproteins it selects for, in order of greatest affinity, are N-Acetyl Glucosamine and N-Acetylneuraminic acid (sialic acid).

All animals, including worms, fish, birds and humans, use N-Acetyglucosamine as a foundational substance for building the various tissues in their bodies, including the bones. The production of cartilage, tendons, and joints depend on the structural integrity of N-Acetylglucosamine. The mucous known as the glycocalyx, or literally, “sugar coat” is secreted in humans by the epithelial cells which line all the mucous membranes, from nasal cavities to the top to the bottom of the alimentary tube, as well as the protective and slippery lining of our blood vessels. The glycocalyx is composed largely of N-Acetylglucosamine and N-Acetylneuraminic acid (also known as sialic acid), with carbohydrate end of N-Acetylneuraminic acid of this protective glycoprotein forming the terminal sugar that is exposed to the contents of both the gut and the arterial lumen (opening).

WGA is an exceedingly small glycoprotein (36 kilodaltons)

Lectins … are notoriously dangerous even in minute doses and can be fatal when inhaled or injected directly into the bloodstream. According to the U.S. Centers for Disease Control it takes only 500 micrograms (about half a grain of sand) of ricin (a lectin extracted from castor bean casings) to kill a human.

The main source of glucosamine on the market is from the N-Acetylglucosamine rich chitin exoskelotons of crustaceans, like shrimp and crab. Glucosamine is used for reducing pain and inflammation. We do not have a dietary deficiency of the pulverized shells of dead sea critters, just as our use of NSAIDs is not caused by a deficiency of these synthetic chemicals in our diet. When we consume glucosamine supplements, the WGA, instead of binding to our tissues, binds to the pulverized chitin in the glucosamine supplements, sparing us from the full impact of WGA.

At exceedingly small concentrations (nanomolar) WGA stimulates the synthesis of pro-inflammatory chemical messengers (cytokines) includingInterleukin 1, Interleukin 6 and Interleukin 8 in intestinal and immune cells. WGA has been shown to induce NADPH-Oxidase in human neutrophils associated with the “respiratory burst” that results in the release of inflammatory free radicals called reactive oxygen species. WGA has been shown to play a causative role in patients with chronic thin gut inflammation.

WGA induces thymus atrophy in rats and may directly bind to, and activate, leukocytes. Anti-WGA antibodies in human sera have been shown to cross-react with other proteins, indicating that they may contribute to autoimmunity. Indeed, WGA appears to play a role in the pathogenesis of celiac disease (CD) that is entirely distinct from that of gluten, due to significantly higher levels of IgG and IgA antibodies against WGA found in patients with CD, when compared with patients with other intestinal disorders. These antibodies have also shown not to cross-react with gluten antigens

WGA can pass through the blood brain barrier (BBB) through a process called “adsorptive endocytosis” and is able to travel freely among the tissues of the brain which is why it is used as a marker for tracing neural circuits. WGA’s ability to pass through the BBB, pulling bound substances with it, has piqued the interest of pharmaceutical developers who are looking to find ways of delivering drugs to the brain. WGA has a unique binding affinity for N-Acetylneuraminic acid, a crucial component of neuronal membranes found in the brain, such as gangliosides which have diverse roles such as cell-to-cell contact, ion conductance, as receptors, and whose dysfunction has been implicated in neurodegenerative disorders. WGA may attach to the protective coating on the nerves known as the myelin sheath and is capable of inhibiting nerve growth factor which is important for the growth, maintenance, and survival of certain target neurons. WGA binds to N-Acetylglucosamine which is believed to function as an atypical neurotransmitter functioning in nocioceptive (pain) pathways.

WGA has been demonstrated to be cytotoxic to both normal and cancerous cell lines, capable of inducing either cell cycle arrest or programmed cell death (apoptosis).

WGA may prevent DNA replication. WGA binds to polysialic acid (involved in posttranslational modifications) and blocks chick tail bud development in embryogenesis, indicating that it may influence both genetic and epigenetic factors.

WGA has also been shown to have an insulin-mimetic action, potentially contributing to weight gain and insulin resistance

WGA induces platelet activation and aggregration. WGA has a potent, disruptive effect on platelet endothelial cell adhesion molecule-1, which plays a key role in tissue regeneration and safely removing neutrophils from our blood vessels.

WGA causes increased shedding of the intestinal brush border membrane, reduction in surface area, acceleration of cell losses and shortening of villi, via binding to the surface of the villi. WGA can mimic the effects of epidermal growth factor (EGF) at the cellular level, indicating that the crypt hyperplasia seen in celiac disease may be due to the growth-promoting effects of WGA. WGA causes cytoskeleton degradation in intestinal cells, contributing to cell death and increased turnover. WGA decreases levels of heat shock proteins in gut epithelial cells leaving these cells less well protected against the potentially harmful content of the gut lumen.

However, it makes sense to be concerned about foods other than wheat:

There are other lectins in the Western diet that have properties similar to wheat lectin (WGA), namely, “chitin-binding lectins.”  Remember, “chitins” are long polymers of n-acetyl-glucosamine, the primary binding target of wheat lectin. Wheat lectin and “chitin-binding lectin” therefore share functional similarities. 

More here

Antigenically similar chitin-binding lectins are present in the embryos of wheat, barley, and rye, members of the Triticeae tribe of the grass family (Gramineae).

Similar lectins were not detected in oats and pearl millet, members of other tribes of the Gramineae. Rice, a species only distantty related to wheat, contains a lectin that is antigenically similar to the other cereal lectins and located at the periphery of embryonic roots and throughut the coleoptile.

Tomato and potato lectins are mentioned here and here. Here is some more on tomato lectins:

Intranasal delivery of tomato lectin (LEA) elicited a strong lectin-specific systemic and mucosal antibody response but only weakly potentiated the response to co-delivered OVA. In contrast, administration of wheatgerm agglutinin (WGA) or Ulex europaeus lectin 1 (UEA-I) with OVA stimulated a serum IgG response to OVA while the lectin-specific responses (particularly for WGA) were relatively low.

However, there is some evidence tomatoes actually reduce inflammation because they also contain a number of compounds that are beneficial to health.

Of course tomatoes and the nightshade family also contain alkaloids which have negative effects on health. These amounts are clearly sufficiently low that we don’t notice it much.

Four kinds of alkaloids in the Solanaceae family include the steroid alkaloids (the alkaloid found in most nightshade foods), tropane, pyrrolizidine and indole alkaloids. Steroid alkaloids have been shown to block certain nerve activity that can, at high levels, cause muscle shaking, paralysis and respiratory difficulty. They have also been associated with inflammation, particularly in the joints. Finally, some nightshade foods like eggplant and tomato contain trace amounts of nicotine.

The essential point of the paleolithic diet is that humans didn’t discover that cooking made grains, beans, potatoes and other foods edible until 10,000 years ago. Since it takes 100,000 years to adapt to a new food group, it is likely that our bodies can not handle these foods well.

Tomatoes are actually interesting because they are in the nightshade family - the same family as potatoes. Here is some tomato history.

The Tomato History has origins traced back to the early Aztecs around 700 A.D; therefore it is believed that the tomato is native to the Americas. It was not until around the 16th century that Europeans were introduced to this fruit when the early explorers set sail to discover new lands. 

More here

Genetic evidence shows the progenitors of tomatoes were herbaceous green plants with small green fruit and a center of diversity in the highlands of Peru.

So the idea is that tomatoes are a relatively new, foreign fruit, more related to the foods that are bad for us than the foods that are good for us. The prominent members of the nightshade family are potato (except sweet potatoes and yams), tomato, eggplant, tobacco, and peppers (except black and white pepper) (includes paprika, chipotle, & cayenne).

It’s possible that we could discover that tomato lectins are not as harmful as other lectins, but I feel that given the large number of fruits out there, cutting out one is no big deal.

Tomatoes are famous for lycopene, but watermelon and papaya are also great sources there.

Source μg/g wet weight

Raw tomato 8.8–42

Watermelon 23–72

Pink grapefruit 3.6–34

Pink guava 54

Papaya 20–53

Some of the other effects of lectins are interesting to me. For example, here is a possible link between lectins and psoriasis. Of course grains have a number of anti-nutrients and while researching this, I came across benzoxazinoids, which are contained in wheat, maize, and rye, and apparently can be somewhat mutagenic.

Of course this is also an argument in favor of cutting out any type of meat that are fed grains. So the eliminates any meat that’s not grass fed. It also eliminates eggs, as almost all chickens are fed grains of some sort, even so-called pastured chickens. I thought this was interesting:

I’ve read anecdotes from celiacs who have reacted to eggs from chickens fed wheat, but not from chickens fed corn.

It is my bet that there are lot of problems associated with eggs that stem directly from the fact that modern chickens are fed wheat, soy and corn - 3 foods disallowed by the paleolithic diet. Just as meat is unhealthy, partly because of what cows are fed, in comparison to grass fed beef, my bet is eggs are not as healthy as they might be if chickens ate insects and other foods for which they were evolutionarily designed.

Reducing fasting insulin levels has been linked to better health and longevity. Here's how you do it.

A number of studies have shown that high carbohydrate diets increase plasma triglyceride levels, VLDL cholesterol, insulin and glucose concentrations in NIDDM40,41 and in post-menopausal women

Diets high in saturated fats and trans-fatty acids have been shown to decrease membrane fluidity and decrease insulin receptor binding, thus promoting insulin resistance. Interestingly, a high omega-6:omega-3 EFA diet is also detrimental to insulin receptor sensitivity. …

… Very good studies indicate that trans fats interfere with insulin receptors and therefore with insulin resistance.

Physical activity reduces insulin resistance.

Weight loss reduces insulin resistance.

Alcohol reduces insulin resistance.

Minerals such as magnesium, calcium, potassium, zinc, chromium, and vanadium appear to have associations with insulin resistance or its management. Amino acids, including L-carnitine, taurine, and L-arginine, might also play a role in the reversal of insulin resistance. Other nutrients, including glutathione, coenzyme Q10, and lipoic acid, also appear to have therapeutic potential.?

There is also evidence that the amount and range of carotenoid-like pigments in an individual’s blood is inversely related to fasting serum insulin levels,65 suggesting a diet low in vegetables might contribute to insulin resistance.

Dietary micronutrient deficiencies might also promote insulin resistance. Chief among these deficiencies appear to be minerals including calcium, magnesium, potassium, chromium, vanadium, and zinc.68-74 Intake of sodium, either too high or two low, appears to negatively impact insulin sensitivity.

Linoleic acid, the major n-6 fatty acid, is metabolized into pro-inflammatory arachidonic acid, which, in turn, gives rise to leukotrienes and protaglandins. N-3 fatty acids, found in plants and in fish, reduce the levels of arachidonic acid, thereby lowering inflammatory mediator concentrations and increasing insulin sensitization.

a saturated fat metabolite called ceramide contributes to the development of insulin resistance. … Ceramide is a lipid molecule made in the body from something called sphingosine and a fatty acid (which could be oleic acid, a so-called good fatty acid). This molecule is used to make sphingomyelin, which is one of the structural elements in the lipid bilayer, as well as being a cellular signal molecule. Sphingomyelin is one of the lipid building blocks of the myelin sheath so important for nerves.

Aging and Longevity – Methylation

Methylation enables the body to:

  • Detoxify toxins within the cell
  • Repair damaged DNA
  • Create new cells

If the cycle of methylation is not working well a dangerous substance called homocysteine accumulates in the blood. High homocysteine levels cause serious damage to the cells and the DNA. This leads to premature aging – and premature death.

High homocysteine is closely involved in:

  • Heart and artery disease
  • Diabetes
  • Alzheimer’s disease
  • Various types of cancer
  • Depression
  • Parkinson’s disease
  • Low thyroid function
  • IBS (inflammatory bowel syndrome)
  • ME (Myalgic encephalitis)

and other serious degenerative diseases.

For example a raised homocysteine level can easily double or even quadruple the chances of atherosclerosis and other artery problems, leading to serious illness or death.

To improve methylation and thus reduce homocysteine there are two approaches:

To increase the elements in the blood, which supply the necessary methyl groups – primarily TMG (trimethylglycine) and SAM-e (S-adenosyl-methionine), and:

To make sure the nutrients, which enable methylation to take place all present in sufficient quantities – these are primarily vitamin B12, folic acid and zinc.

The target level of homocysteine in the blood is 6.3 µmol per liter of blood or less. If as high as 15 µmol per liter – and this level is not rare – the risk of coronary artery disease is quadrupled. A simple blood test will show the level of homocysteine present.

I’ve always taken very few vitamins, together with a multi-mineral - but never supplements. I currently take vitamin D, dessicated liver for b12, and then calcium (because I don’t feel like gnawing on bones or grinding egg shells - although perhaps they might be better sources) and a multi-mineral (to be safe). I get tons of folic acid from the food I eat. Zinc? Well that’s a reason to eat more oysters. Dunno. Somewhat skeptical of supplements. Beef liver actually contains folate as well - even though it’s not listed on my supplement data, so I’m not sure about the extent to which  it survives in pill form. Anyway, this to me is a very interesting angle on eating healthily.

Your Body Shape and Heart Disease

A major new analysis challenges the long-held idea that obese people who carry their extra weight mainly around the middle — those with an “apple” shape — are at greater risk for heart disease than “pears,” whose fat tends to cluster on their thighs and buttocks.

The new report, published online on March 11 in The Lancet, pooled data from 58 studies about more than 220,000 people,mean age of 58. During the time they were followed, more than 14,000 suffered a heart attack or stroke. Conventional risk factors like blood pressure, cholesterol, diabetes and smoking were accurate predictors of a heart attack or stroke, but additional information about weight or body shape (ascertained by measuring waist circumference or waist-to-hip ratio) did not improve the ability to predict risk.

What is being said here, in my opinion, is that there are some people who are pear shaped or fat - and for whatever reason they are actually quite healthy  - and don’t have any of the above risk factors for heart disease. So despite being fat or pear shaped, they have low blood pressure, cholesterol, no diabetes, etc.

It’s an interesting exception. 

Blueberries combat diabetes, metabolic syndrome, cancer

In a recent double-blind, placebo-controlled study, 32 obese, insulin-resistant (pre-diabetic) adult men and women drank smoothies made with freeze-dried blueberry powder for six weeks. A placebo control group consumed smoothies without blueberry extracts.

With no changes in body weight or composition compared to controls, the blueberry group showed a statistically significant and much greater improvement in insulin sensitivity (22.2% plus or minus 5.8%) versus the placebo arm (4.9% plus or minus 4.5%).

Another study examined 48 individuals afflicted with metabolic syndrome, the constellation of pathologies that includes high blood pressure, central obesity (around the abdomen), elevated blood glucose, insulin resistance, and unfavorable lipid profiles (high LDL cholesterol and triglycerides and low HDL cholesterol). In this randomized, controlled trial, participants consumed a freeze-dried blueberry drink or an equal amount of fluids. After eight weeks, the blueberry group experienced greater decreases in systolic and diastolic blood pressure readings, compared with the control group. The test group also exhibited lower levels of oxidized LDL and other inflammatory markers associated with the metabolic syndrome.

On cancer…

 

Researchers have discovered that blueberry anthocyanins combat cancer development in three distinct ways:

  1. They inhibit the creation of new blood vessels essential to tumor growth (angiogenesis).19
  2. They impede the spread of tumor cells to different locations in the body (metastasis).19
  3. They stimulate cellular maturation, or differentiation, into less injurious or malignant forms.19

Blueberries are one of the few foods that have a meaningfully positive effect on your brain. Foods that do this many good things are rare. Putting everything together it’s a pretty convincing argument to eat blueberries regularly.

Milk - not doing a body good. Exploring the connection with stress, histamine, heart disease, diabetes, autism/asd, schizophrenia, more…

Milk is a sedative:

For generations, mothers have given their children a warm glass of milk before bed as a way to help them fall asleep. As far back as 1934, this home remedy gained scientific validation when it was observed that people who ate milk and cornflakes were more likely to enjoy a full night of uninterrupted sleep.

In 1997, pediatric researchers added to the evidence by demonstrating that newborns given an infant formula containing milk fell asleep not solely due to nursing and being held, but owing specifically to something in milk itself.

In 2000, researchers identified what that “something” was. It turns out that nutrients found in cow’s milk called bioactive peptides (chains of amino acids) exert a sedative effect on the brain and induce sustained sleep patterns.

These bioactive milk peptides have since been shown to act on the brain’s GABA-A receptors, the same mechanism of action that makes the class of sedatives known as benzodiazepines so effective. The advantage of milk peptides, of course, is that they induce relaxation and sleep without the side effects associated with long-term benzodiazepine use.

In pre-clinical models, milk peptides markedly reduce anxiety and improve sleep in animals subjected to chronic stress.

In human studies, a proprietary bioactive milk peptide compound used widely in Europe has been shown to effectively induce relaxation, leading not only to deeper, more restorative sleep, but also to substantial improvements across a wide range of stress markers.

The article cited above goes on to talk about how their milk extract is marvelous, and how it succeeds in reducing stress in additional clinical trials.

Milk contains casein…

Casein has been documented to break down in the stomach to produce the peptide casomorphin, an opioid that acts as a histamine releaser. 

What are the effects of this histamine release?. It’s complicated because there are multiple receptors for it:H1,H2,H3,H4, each of which do something different when histamine is released and stimulates them:

  • [H1] Histamine heightens allergic reactions and those you experience during colds and allergies. It makes you more likely to cough and sneeze. On your skin it makes you more likely to have eczema and get hives and it makes insect bites more itchy. For your stomach, it heightens nausea and motion sickness. It also wakes the body up, perhaps to deal with these perceived problems.
  • [H2] Histamine dilates your blood vessels, and is involved in erections. It also inhibits part of your immune system (antibody synthesis, T-cell proliferation and cytokine production).
  • [H3] Makes you sleepy and lessens pain perception. So H1 makes you awake, but H3 makes you sleep, so for whatever reason milk’s action on the H3 histamine receptors appear to override its effects on H1 receptors. 
  • [H4] Active in bone marrow and the immune system.

So how to make sense of these different ways in which Histamine acts? As this site says,

Histamine is an immune system mediator or, more simply, a chemical messenger that helps direct your body’s response to a foreign invader. 

It essentially tells your body, get overly active in fighting off a perceived acute disease or threat of some sort - and get a little bit stressed out about it - and lower general immunity, relax with respect anything other than this acute problem, and go to sleep.

So histamine takes a small issue - whether it’s bee pollen or some other allergen, and makes your body perceive it to be a huge problem and totally focuses your body on defending itself from said problem. My guess is it does the same thing in your brain personality-wise. It makes you more likely to recognize something small as a major acute problem which must be dealt with immediately. In the absence of a perceived stress - which would probably be amplified by the histamine - it is likely sedative.

Milk is bad in other ways….

Milk contains a small amount of actual morphine - which in itself is interesting.

Casein breaks down down into a few things in your gut, one of which is BCM-7.

BCM-7 has been implicated in the development of both ischaemic heart disease (IHD)  and diabetes mellitus type I (DM-I) (Elliott et al. 1999; Thorsdottir et al. 2000; McLachlan 2001; Laugesen and Elliott 2003; Tailford et al. 2003)

For IHD, BCM-7 could act on LDL through peroxidation of the lipids within LDL  through a tyrosyl radical mechanism of action (Elliott at al. 1999; Heinecke et al. 1999).

For DM-I…BCM-7 suppresses immune defense mechanisms by inhibiting the incorporation of thymidine into lymphocyte DNA replication thereby inhibiting lymphocyte proliferation (Elitsur and Luk 1991). This generates an immune vulnerability (in the case of DMI) to a certain class of enteroviruses that are still being researched as they may have potential key roles in the damage done to pancreatic beta cells (Graves et al. 1997). Through BCM-7 compromising the immune system, the system is more vulnerable to all kinds of pathogenic infections. 

 BCM-7 acts on the mu-opioid receptor which in turn causes the release of histamine (Kostyra et al. 2004)

The suspected heart disease and diabetes mechanism has everything to do with the protein in milk (Casein which breaks down into BCM-7) and little to do with the saturated fat in the milk. More on that correlation.

Milk causes a release of intestinal mucous.

Like heroin or codeine, casomorphins slow intestinal movements and have a decided antidiarrheal effect. The opiate effect may be why adults often find that cheese can be constipating, just as opiate painkillers are.

More on that release of intestinal mucous.

There is some evidence that casein and gluten (a milk protein) worsen autism, and move you along the autistic scale.

More on autism and heart disease/diabetes:

Studies involving large samples of  patients with autism, schizophrenia, or mania found that over 90 % of those tested had high levels of the milk protein beta-casomorphine-7 in their blood and urine and defective enzymatic processes for digesting milk protein(24,25,27), and similarly for the corresponding enzyme needed to digest wheat gluten(24,26). Like casein, gluten breaks down into molecules with opioid traits, called gluteomorphine or gliadin. As with caseomorphin, it too can retain biological activity if the enzymes needed to digest it are not functioning properly..

In hydrolysed milk with variant A1 of beta-casein, BCM-7 level is 4-fold higher than in A2 milk.  Variants A1 and A2 of beta-casein are common among many dairy cattle breeds. A1 is the most frequent in Holstein-Friesian (0.310–0.660), Ayrshire (0.432–0.720) and Red (0.710) cattle. In contrast, a high frequency of A2 is observed in Guernsey (0.880–0.970) and Jersey (0.490–0.721) cattle(92). In children with autism, most of whom have been found to have been exposed to high levels of toxic metals through vaccines, mother’s dental amalgams, or other sources;   higher levels ofBCM-7 is found in the blood(24-26). 

Epidemiological evidence from New Zealand claims that consumption of beta-casein A1 is associated with higher national mortality rates from ischaemic heart disease. It appears that the populations that consume milk containing high levels of beta-casein A2 have a lower incidence of cardiovascular disease and type 1 diabetes. 

A double blind study using a potent opiate antagonist, naltrexone (NAL), produced significant reduction in autistic symptomology among the 56% most responsive to opioid effects(28). 

Of course you’ll get less heart disease in a population that drinks a form of milk with less beta-casein, but of course one might postulate that heart disease would be further reduced with casein and milk elimination.