Recent in vitro and animal studies have reported estrogen-like activity of chemicals used in sunscreen preparations. We investigated whether the three sunscreens benzophenone-3 (BP-3), octyl-methoxycinnamate (OMC), and 3-(4-methylbenzylidene) camphor (4-MBC) were absorbed and influenced endogenous reproductive hormone levels in humans after topical application. In this 2-wk single-blinded study 32 healthy volunteers, 15 young males and 17 postmenopausal females, were assigned to daily whole-body topical application of 2 mg per cm2 of basic cream formulation without (week 1) and with (week 2) the three sunscreens at 10% (wt/wt) of each. Maximum plasma concentrations were 200 ng per mL BP-3, 20 ng per mL 4-MBC, and 10 ng per mL OMC for females and 300 ng per mL BP-3, 20 ng per mL 4-MBC, and 20 ng per mL OMC for men. All three sunscreens were detectable in urine. The reproductive hormones FSH, LH were unchanged but minor differences in testosterone levels were observed between the 2 wk. A minor difference in serum estradiol and inhibin B levels were observed in men only. These differences in hormone levels were not related to sunscreen exposure.
They found that if they took otherwise healthy people and put them in an environment where they could sleep up to 14 hours per day, they slept well over their baseline amount (as if working off a sleep debt) for as long as 3 weeks. The first few days they would sleep 10-11 hours a night, then after a couple of weeks it would be 9 hours - only after 3-4 weeks did it subside to the final equilibrium of ~8.5 hours a night, at which point the subjects reported that they felt terrific.
There are more recent, similar studies done at Stanford on athletes that show that in a similar environment, sprint times continued to decrease as much as two months into the study.
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.
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.
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
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.
Considering that the oldest farmers started their occupational exposure in the 1970s and that latency is important, pesticides used in vineyards during the 1970s and 1980s are of primary concern for the effects we observed. During that period, the most probable fungicides used were dithiocarbamates, phtalimides, dicarboximides, triazoles and inorganic substances (copper, sulphate, arsenic) with, to a lesser extent, insecticides (organophosphates, organochlorines and carbamates) and some herbicides (triazines or sulfamides)
Follow-up of the PHYTONER cohort showed lower cognitive performances in pesticide-exposed subjects. Among the seven cognitive tests significantly associated with pesticide exposure, three have a cognitive speed component: (i) the TMT, also implying a selective attention component, (ii) the FTT, a very simple motor speed test with a strategic component and (iii) the IST, a semantic verbal fluency test which implies integrity of semantic memory, as well as strategic search, working memory and a speed component. Performance on two of these tests with a speed component have already been found to be associated with chronic pesticide exposure (the TMT22–24) as has often been found with other cognitive speed tests, such as the TMT part B22 25 26 and the Digit Symbol Substitution Test.22 24 25 27 28 The most strongly associated test, the BVRT, is a visual working memory test, which also implies selective attention and inhibition, and this test and other quite similar ones have already been shown to be associated with chronic pesticide exposure.22 29–32 The second most associated measure is the number of good answers on the Stroop interference test, implying selective attention and inhibition of an automatic response. Finally, performances on two episodic memory tests were also associated with pesticide exposure, as was the case with the Rey Auditory Verbal Learning Test in another study.32 Associations between pesticide exposure and test results were very strong with ORs for having a performance in the lower quarter of the distribution exceeding 5 for the visual working memory test (the BVRT) and 1 for the cognitive speed test (the TMT) and being even stronger for some cognitive measures if one considers the risk to be in the lower 10% of performances, with a risk multiplied by more than eight for the BVRT and more than 10 for the ST. No clear dose–effect relationship was observed between the directly and indirectly exposed. The evolution of performances over a 4–5-year period demonstrated that exposed subjects generally had the greatest decrease: on the MMSE they had a 1.97 risk of lowering their score by two points between baseline and follow-up compared to non-exposed subjects, and a 1.64 risk of lowering their score by three points. This result is particularly striking in view of the short duration of follow-up and the relatively young age of the participants.
A longitudinal study of performances in a French population aged 65 and over without dementia showed a slight decline over 5 years only in tests with a speed component, but not on the MMSE or the BVRT.33 The observed decline in pesticide-exposed subjects on the MMSE, a composite measure reflecting global cognitive deterioration, cannot therefore be considered a sole effect of ageing, especially as the subjects were relatively young.
Pesticides can even strip away the protective effect of education
We also observed a stronger impact of pesticide exposure in groups who had protective characteristics at baseline with regard to cognitive performances (highly educated, no alcohol consumption, women) even if these groups had and continued to have a higher performance than others. Several studies have demonstrated that highly educated people have a lower risk of Alzheimer’s disease and dementia, which is often explained by a hypothetic ‘reserve capacity’.34 35 This ‘reserve’ might explain why their performances were better than those of the less educated subjects at baseline. They may initially resist pesticide exposure better, but their accelerated decline showed that prolonged exposure combined with ageing may considerably reduce their protective factors.
How fructose and HFCS increase uric acid and give you high blood pressure
So this article below introduces the idea of fructose and its effects on Uric acid. It also mentions some things I’ve talked about before about how fructose doesn’t provoke an insulin response.
Fructose elevates uric acid, which decreases nitric oxide, raises angiotensin, and causes your smooth muscle cells to contract, thereby raising your blood pressure and potentially damaging your kidneys. Increased uric acid also leads to chronic, low-level inflammation, which has far-reaching consequences for your health. For example, chronically inflamed blood vessels lead to heart attacks and strokes; also, a good deal of evidence exists that some cancers are caused by chronic inflammation.
Fructose does not appropriately stimulate insulin, which in turn does not suppress ghrelin (the “hunger hormone”) and doesn’t stimulate leptin (the “satiety hormone”), which together result in your eating more and developing insulin resistance.
glucose actually accelerates fructose absorption, making the potential health risks from HFCS even more profound.
There are more than 3,500 articles to date showing a strong relationship between uric acid and obesity, heart disease, hypertension, stroke, kidney disease, and other conditions. In fact, a number of studies have confirmed that people with elevated serum uric acid are at risk for high blood pressure, even if they otherwise appear to be perfectly healthy.
Uric acid levels among Americans have risen significantly since the early half of the 20th Century. In the 1920s, average uric acid levels were about 3.5 ml/dl. By 1980, average uric acid levels had climbed into the range of 6.0 to 6.5 ml/dl and are probably much higher now.
How Does Your Body Produce Uric Acid?
It’s a byproduct of cellular breakdown. As cells die off, DNA and RNA degrade into chemicals called purines. Purines are further broken down into uric acid.
Fructose increases uric acid through a complex process that causes cells to burn up their ATP rapidly, leading to “cell shock” and increased cell death. After eating excessive amounts of fructose, cells become starved of energy and enter a state of shock, just as if they have lost their blood supply. Massive cellular die-off leads to increased uric acid levels.
According to Dr. Johnson1, sugar activates its own pathways in your body—those metabolic pathways become “upregulated.” In other words, the more sugar you eat, the more effective your body is in absorbing it; and the more you absorb, the more damage you’ll do.
You become “sensitized” to sugar as time goes by, and more sensitive to its toxic effects as well.
The flip side is, when people are given even a brief sugar holiday, sugar sensitization rapidly decreases and those metabolic pathways become “downregulated.” Research tells us that even two weeks without consuming sugar will cause your body to be less reactive to it.
This video adds a bit. Here are my very rough notes, which may be imperfect.
Fructose is 7 times more likely to brown, and form AGE -advanced glycation end products than glucose
Fructose does not suppress ghrelin (because it does not cause an insulin spike).
If you eat glucose it gets used all over your body. 80% of glucose gets used in the body. 20% gets used in the liver and most gets converted to glycogen. Your liver can store unlimited amounts of glycogen without toxicity.
Some portion of the glucose will get converted into fat/VLDL. (maybe 0.5% depending)
When you drink alcohol.
80% of ethanol calories hit the liver.
Ethanol generates reactive oxygen species which damage proteins in the liver.
You get a lot of VLDL /fat from ethanol.
100% of fructose gets metabolized by the liver.
Uric acid gets created as a waste product as fructose is metabolized.
Uric acid contributes to gout.
Uric acid blocks the synthesis of Nitric Oxide. Nitric Oxide lowers blood pressure. So the result is that your blood pressure rises.
Another fructose by-product is xylose-5-phosphate, which stimulates pp2a which then activates lipogenesis (new fat making).
With glucose almost none of it ends up as fat. With fructose 30% ends up as fat.
In 6 days of med students drinking lots of fructose, triglyceride levels doubled.
One of the byproducts of fructose metabolism limits the effectiveness of insulin in the liver. via JNC1 IRS1
The higher insulin levels go, the less well the brain recognizes leptin. So the brain gets confused - thinks it’s starving despite high fat stores.
Fiber is the antidote for high sugar levels. Fiber reduces the rate of intestinal carbohydrate absorption. Downside: “In life you’ve got 2 choices - fat or fart.”
Fiber increases the speed of transit of intesinal contents to the ileum which raises PYY and produces a satiety signal.
Inhibits absorption of some free fatty acids in the colon which are metabolized by colonic bacteria to short chain fatty acids which suppress insulin levels.
Gout is a kind of arthritis that occurs when uric acid builds up in the joints.
Here is a good powerpoint presentation on what happens to fructose in liver cells.
Fructose + ATP => Fructose1P + ADP
As wikipedia explains, fructose is absorbed more rapidly if glucose is present, leading to a more rapid increase in triglyceride levels and the by products of fructose metabolism:
Studies show the greatest absorption rate occurs when glucose and fructose are administered in equal quantities. When fructose is ingested as part of the disaccharide sucrose, absorption capacity is much higher because fructose exists in a 1:1 ratio with glucose. It appears that the GLUT5 transfer rate may be saturated at low levels, and absorption is increased through joint absorption with glucose. One proposed mechanism for this phenomenon is a glucose-dependent cotransport of fructose.
This is yet another reason to limit fructose consumption. Please see this post of mine on fructose if you haven’t already.
Research by Kuberski6 identified the sugars contained in coconut water, detecting glucose, sucrose and fructose in the proportion of approximately 50, 35 and 15%, respectively, but their study did not relate whether these proportions remained constant during different months. The current study found that the proportions of these sugars varied depending on the stage of maturation of the coconuts: glucose, from 34 to 45%; sucrose, from 53 to 18% and; fructose, from 12 to 36%.
150 lb Body Builders eat 3 lbs of meat equivalent per day; wow!
It has been speculated that the minimum protein intake required to promote muscle gain is about 1g/per pound body weight. Bodybuilders often consume 2g/per pound body weight per day. This means that a 150lb bodybuilder may consume 300g protein (equivalent to three pounds of meat or 50 eggs) per day. That’s a lot of protein to shove in…
The incidence of Food Allergy in Australian Children
(Based on David Hill’s report, Royal Children Hospital, Melbourne)
Cow’s Milk 2%
Sesame Seed 0.42%
Cashew Nut 0.33%
Brazil Nut 0.07%
Multiple Food Allergies
Based on David Hill’s study above, between 50% and 75% of children with cow’s milk allergy (CMA) have hypersensitivity to other foods.
Incidence of adverse reactions to other foods in 100 children with CMA:
(Percentage of CMA children with other adverse reaction to foods)
Casein Hydrosylate 22%
(Reference: Bishop JM, Hill DJ et al, Natural history of cow’s milk allergy: clinical outcome. J Paediatrics 1990; 116:862)
So 18% of those with cow’s milk allergy have an allergy to bananas, that’s about 0.36% of children. Most children out grow those allergies as well.
One of the arguments made by those who support the paleolithic diet revolves around food allergies. While I support so many of the recommendations of the paleolithic diet food allergies are not necessarily the strongest evidence. They are one data point. I do think it’s significant that so many are allergic to milk.
Most people who are allergic to hen’s eggs have antibodies which react to one of four proteins in the egg white: ovomucoid, ovalbumin, ovotransferrin, and lysozyme; ovomucoid, also called Gal d 1, is the most common target of immune system attack. The egg yolk contains several potential antigens: livetin, apovitillin, and vosvetin.
Egg – Always prized, but rarely available until domestication of fowl c. 9500 years ago in Asia. Domestic egg production arrived in Egypt c. 3500 years ago, and Greece c. 2800 years ago.
Thus food allergies to eggs are common because eggs, historically, are rare.
The same site talks about other foods
Eight foods account for over 90% of food allergies in the United States.
Dairy– First unequivocal evidence for consumption c. 7000 years ago in Europe, although since it’s associated with modern pastoralists like theMaasai, it may be somewhat older.
Soy– First domesticated in China c. 5000 years ago, first grown outside southeast Asia c. 2000 years ago. First grown in Europe and America in the 18th century.
Gluten (wheat and related grains)– Grains were first domesticated in the Middle East, c. 12000 years ago…but agriculture didn’t spread beyond the Middle East until c. 5000 years ago.
Peanut– First domesticated c. 7600 years ago in Peru. Confined to South and Central America until the 16th century, when European traders spread them around the world. (Note that the peanut is actually a legume, like the soybean.)
Shellfish– c. 160,000 years ago, South Africa. (Link.)
Tree nut– All common tree nut allergies are, without exception, totrees not native to Africa(walnuts, cashews, almonds, hazelnuts, pine nuts), and modern humans didn’t leave Africa until c. 60,000 years ago. Allergies to native African nuts, such as kola nuts (found in Coca-Cola), and palm nuts (from which palm oil is made), are rare.
Dairy (lactose intolerance) – While approximately 5% of Europeans are lactose intolerant, the figure rises to 75% for Africans and 100% for Native Americans. (Link.) (Note, however, that butter, being essentially pure butterfat with minor impurities, is well-tolerated by everyone without frank allergy.)
It’s difficult to know which fruits you may or may not be slightly allergic to. It’s never good to have small allergic battles waged by your body, unbeknownst to you. However, as I see it fruit has a number of benefits and shouldn’t be excluded out of fear, unless sufficient data can be accumulated on any one fruit. It’s tough to make any diet or nutrition program perfect, and odds you’re going to be the tiniest bit allergic to some of the things you eat without knowing it. It’s a compromise but it’s also reality.
the food has spent between 30 minutes and 2 hours in the stomach and between 2 and 6 hours in the small intestine and 90% of the nutrients have been extracted. The left over material has lots of water and sodium left in it. The body wants to reclaim these substances before defecation; food takes 72 hours to be processed in the large intestine. The jobs of the large intestine are to reclaim the water from the food, reclaim the sodium from the food, and provide healthy bacteria to ferment fiber that has not been digested. This fermentation provides nutrients to keep the cells in the large intestines healthy. Fiber that has not been digested adds bulk to the waste products to facilitate elimination. In summary, at the short end, digestion takes about 75 hours, but it can take up to 80 hours from the time it enters the mouth to the time it leaves the body in the form of stool.
This is relevant because you might want to give your body time to digest nuts which contain phytates before eating vegetables, because the phytates in the nuts could leach mineral content from the vegetables.
This implies that if you wait 2.5 to 8 hours phytates will cease to be an issue because they will be gone from the small intestine where minerals are absorbed. That’s probably overly conservative because it will take time for the vegetables to reach the small intestine, and if vegetables are nearer one end of the small intestine and nuts are nearer they other they likely won’t co-mingle.
Anytime you eat or drink anything that is sugary, the bacteria in your mouth feed on these sugars to make acids. These bacterial acids cause the pH in your mouth to drop below normal levels and make your tooth enamel “softer” and more vulnerable to abrasion. For most people the pH at which your tooth enamel begins to demineralize is about pH ~5.5. The process of bringing your oral pH back to normal is far from immediate and typically takes about 30 minutes, so you should not rely on your saliva alone to reverse these drops in pH.
“Alcohol kills germs. True statement… but an incomplete statement. Generally, 70% alcohol is needed to kill off many “germs” (bacteria/viruses.) Vodka is generally 80 proof = 40% alcohol. Which probably does have some sterilizing effect, but no where near medicinal strength.”—
Paleolithic humans have a median lifespan of 30 to 35 years depending on gender, with a certain stature (body height) and frame size (a loose indicator of strength).
As agriculture is developed (i.e. the diet becomes no longer Paleo), the life expectancy became shorter, and people became shorter with smaller frames.
The life expectancy did not recover until close to 1500 B.C., when it went back up to about 35 to 40 years depending on the gender. However, people continue to remain short with smaller frames.
The life expectancy hovered at around 40 years all the way to some time in the middle of the 20th century. However, people were never again as tall or strong as they were in the Paleolithic times.
Basically, as people transitioned away from a Paleo diet toward a grain-based Neolithic diet, they became weaker and shorter, and died sooner. Some other non-dietary factors that came along much later were able to gradually recover the life expectancy, but not the height and strength.
For those who insist on comparing the life expectancy of Paleolithic hunter-gatherers with that of modern 21st century humans, realize that the differences are due mostly to technology and societal change, not to diet. These include:
Clean and reliable sources of drinking water
Vaccinations, antibiotics, surgeries
Reduced rates of trauma (no longer need to run from predators or to hunt)
food preparation and processing can reduce the provitamin A carotenoid content of foods by up to 90% Deep-frying, prolonged cooking, combining several preparation and processing methods, baking, and pickling (with the possible exception of the pickling of olives) all result in substantial losses of provitamin A carotenoids β-Carotene is up to three times more available from cooked and pureed than from raw carrots and spinach.
I view this as evidence to be careful with prolonged cooking and to cook things quickly if at all possible.
The legal limit, once as high as .15% in some states, is now .08% in all 50 states. Some experts still consider it generous. Reaction time starts to slow at only half that amount, and much of the world sets stricter limits. It’s .02% in China, .03% in most of India and .05% in much of Europe.
Drinkers who think they can tell when they’ve had enough are very often wrong. “Alcohol can affect your reflexes even if you feel fine,” says Samir Zakhari, director of the division of metabolism and health effects at the National Institute of Alcohol Abuse and Alcoholism. That’s a key reason why many experts urge people who plan to drink any amount of alcohol not to drive, and vice versa.
"The liver can only break down the alcohol at the rate of about one drink per hour,"
BAC generally falls by .015% per hour for both men and women—but will rise again if you keep drinking.
Reviewing the birth records of more than 81,000 infants, researchers found that the risk of having a baby born before 30 weeks of gestation increased 128 percent for women who live near the worst traffic-generated air pollution.
In addition, preeclampsia increased 42 percent for women who lived in those areas, according to the study, published online in the scientific journal Environmental Health Perspectives. Preclampsia, a serious illness that involves high blood pressure, can endanger the baby and the mother.
Air pollutants from Interstate 10 in Santa Monica extend as far as 2,500 meters — more than 1.5 miles — downwind, based on recent measurements from a research team headed by Dr. Arthur Winer, a professor of environmental health sciences at the UCLA School of Public Health. This distance is 10 times greater than previously measured daytime pollutant impacts from roadways and has significant exposure implications, since most people are in their homes during the hours before sunrise and outdoor pollutants penetrate into indoor environments.
although traffic volumes are lower in the pre-sunrise hours, the air pollution concentrations measured by the team were higher than even those during daytime traffic congestion peaks. Concentrations are higher before sunrise even though emissions are lower because of the unique weather conditions. In the pre-sunrise hours, wind speeds are generally very low, and while the wind direction is somewhat variable, the predominant direction is from the northeast in the winter months and the northwest in the summer months.
This means that areas south of Interstate 10 are generally downwind in the pre-sunrise hours and areas north of the freeway are generally upwind; this is consistent with the observation that vehicle-related pollutants are found much further from the freeway on the south side in the pre-sunrise hours, compared with the north side.
"Our research shows that under the low wind speeds and shallow temperature inversions during the early morning, before sunrise, air pollution from freeways is trapped near the surface, limiting dilution and creating a zone of influence many times greater than during the day,"
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.
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.
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.
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.
A 40-year-old mother has approximately a 6% to 8% risk of giving birth to a child with a birth defect. Since the likelihood of most types of birth defects increases with maternal age, a 44-year-old woman could be assumed to have a risk over 8%.
by the 1980s the antibiotics penicillin and tetracycline were no longer effective against it. Next, gonorrhea resistant to fluoroquinolone antibiotics emerged, leaving only one class of antibiotic drugs, cephalosporins, left to treat it. Now, it looks like the sophisticated bacteria responsible for gonorrhea are mutating again and developing resistance to this last line of treatment. Although cases of cephalosporin-resistant gonorrhea have not yet shown up in the United States, it is already circulating in Japan and Europe — a similar trend to what happened when the last widespread resistance developed.
In intervals of two to five days, the volunteers in the study received one of the following food variants on an empty stomach: (1) raw milk; (2) the same milk conventionally cooked; (3) pasteurized milk; (4) the same raw milks cooked in a microwave oven; (5) raw vegetables from an organic farm; (6) the same vegetables cooked conventionally; (7) the same vegetables frozen and defrosted in a microwave oven; and (8) the same vegetables cooked in the microwave oven. Once the volunteers were isolated, blood samples were taken from every volunteer immediately before eating. Then, blood samples were taken at defined intervals after eating from the above milk or vegetable preparations.
Leukocytes are often signs of pathogenic effects on the living system, such as poisoning and cell damage. The increase of leukocytes with the microwaved foods were more pronounced than with all the other variants. It appears that these marked increases were caused entirely by ingesting the microwaved substances.
Microwaving prepared meats sufficiently to insure sanitary ingestion caused formation of d-Nitrosodienthanolamines, a well-known carcinogen.
Microwaving milk and cereal grains converted some of their amino acids into carcinogens.
Thawing frozen fruits converted their glucoside and galactoside containing fractions into carcinogenic substances.
Extremely short exposure of raw, cooked or frozen vegetables converted their plant alkaloids into carcinogens.
Carcinogenic free radicals were formed in microwaved plants, especially root vegetables.
Decrease in nutritional value
So the first set of studies suggests that the microwave oven creates new substances that our immune system needs to fight against. It sufficiently changes food from something our body is familiar with to something that’s a threat. Chronic inflammation taxes our body and is linked to heart disease, cancer, and a variety of other diseases. The second set of studies are self-explanatory, detailing some of the changes that take place and how microwaves transform foods into carcinogens.
After the oranges are squeezed, the juice is stored in giant holding tanks and, critically, the oxygen is removed from them. That essentially allows the liquid to keep (for up to a year) without spoiling– but that liquid that we think of as orange juice tastes nothing like the Tropicana OJ that comes out of the carton.
When the juice is stripped of oxygen it is also stripped of flavor providing chemicals. Juice companies therefore hire flavor and fragrance companies, the same ones that formulate perfumes for Dior and Calvin Klein, to engineer flavor packs to add back to the juice to make it taste fresh. Flavor packs aren’t listed as an ingredient on the label because technically they are derived from orange essence and oil. Yet those in the industry will tell you that the flavor packs, whether made for reconstituted or pasteurized orange juice, resemble nothing found in nature. The packs added to juice earmarked for the North American market tend to contain high amounts of ethyl butyrate, a chemical in the fragrance of fresh squeezed orange juice that, juice companies have discovered, Americans favor. Mexicans and Brazilians have a different palate. Flavor packs fabricated for juice geared to these markets therefore highlight different chemicals, the decanals say, or terpene compounds such as valencine.
The formulas vary to give a brand’s trademark taste. If you’re discerning you may have noticed Minute Maid has a candy like orange flavor. That’s largely due to the flavor pack Coca-Cola has chosen for it. Some companies have even been known to request a flavor pack that mimics the taste of a popular competitor, creating a “hall of mirrors” of flavor packs. Despite the multiple interpretations of a freshly squeezed orange on the market, most flavor packs have a shared source of inspiration: a Florida Valencia orange in spring.
33 percent of them show signs of body dysmorphic disorder, or BDD, a chronic mental illness characterized by excessive worry over appearance that interferes with daily life. The condition does not improve after plastic surgery, and oftentimes, symptoms worsen post-surgery.
Symptoms of BDD include extreme self-consciousness, excessive grooming, frequent examination in the mirror or avoiding mirrors all together and steering clear of social situations because of one’s appearance.
As Stephan highlights, one study showed that 29% of asymptomatic (read: not celiac) people nonetheless tested positive for anti-gliadin IgA in their stool. Anti-gliadin IgA is an antibody produced by the gut, and it remains there until it’s dispatched to ward off gliadin – a primary component of gluten. Basically, the only reason anti-gliadin IgA ends up in your stool is because your body sensed an impending threat – gluten. If gluten poses no threat, the anti-gliadin IgA stays in your gut. And to think, most Americans eat this stuff on a daily basis.
I recently discovered the work of Dr. Kenneth Fine of EnteroLab. He has developed an assay that detects anti-gliadin IgA in stool. Gliadin is one of the problematic proteins in gluten that is implicated in gluten sensitivity. Dr. Fine has been conducting informal research using his fecal anti-gliadin IgA test (data here). He has found that:
100% of untreated celiac patients are antigliadin IgA positive by fecal test, compared to only 76% by blood (n= 17).
76% of microscopic colitis (a type of chronic diarrhea) patients are positive by the fecal test, compared to 9% by blood (n= 57).
57% of symptomatic people (digestive problems?) are positive by the fecal test, compared to 12% by blood (n= 58).
62% of people with autoimmune disease are positive by the fecal test.
29% of asymptomatic (healthy) people are positive by the fecal test, compared to 11-12% by blood (n= 240).
Baby and cow feces are 0% positive by the stool assay.
It gets worse. Gluten sensitivity is determined in large part by genetics. A gene called HLA-DQ is intimately involved. It encodes a protein that is expressed on the surface of cells, that serves to activate immune cells when certain foreign substances are present. Different versions of the gene are activated by different substances. HLA-DQ2 and HLA-DQ8 are classically associated with celiac disease. Roughly 42% of the US population carries DQ2 or DQ8. According to Dr. Fine, every allele except DQ4 has some association with gluten-related problems! Only 0.4% of the U.S. population carries HLA-DQ4 and no other allele. in a preliminary study… Researchers took gut biopsies from celiac patients and asymptomatic controls. Five out of six asymptomatic controls showed elevated interleukin-15, a marker of innate immune activation, upon exposure to gliadin. An activated innate immune system (commonly called ‘inflammation’) is associated with a wide array of chronic diseases, from obesity to cancer to cardiovascular disease. Inflammatory cytokines are elevated in celiac patients and may play a role in their bone pathology.
“Whenever you feel tempted to pop a pimple, control the urge. “Picking can actually make the acne worse and lead to permanent scarring,” Stein says. “Better to leave it alone.” Instead of popping pimples, try an over-the-counter pimple remedy containing benzoyl peroxide or salicylic acid. If that doesn’t clear up your breakouts, call your dermatologist.”—How to Damage Your Skin
58 empirical reports on autism and heavy metal toxins, 43 suggest some link may be present, while 13 reports found no link
Mercury is a ubiquitous source of danger in fish, drugs, fungicides/herbicides, dental fillings, thermometers, and many other products. Elevated Hg concentrations may remain in the brain from several years to decades following exposure.
HFCS has been shown in certain studies to cause more harm than cane sugar. ”Rats with access to high-fructose corn syrup gained significantly more weight than those with access to table sugar, even when their overall caloric intake was the same. “ 
"In addition to causing significant weight gain in lab animals, long-term consumption of high-fructose corn syrup also led to abnormal increases in body fat, especially in the abdomen, and a rise in circulating blood fats called triglycerides. " 
I found this convincing, because it compares the effect of sucrose and HFCS specifically; it doesn’t just study the effect of HFCS in isolation:
"The first study showed that male rats given water sweetened with high-fructose corn syrup in addition to a standard diet of rat chow gained much more weight than male rats that received water sweetened with table sugar, or sucrose, in conjunction with the standard diet. The concentration of sugar in the sucrose solution was the same as is found in some commercial soft drinks, while the high-fructose corn syrup solution was half as concentrated as most sodas."  
At the same time, there is a lot of literature that claims that HFCS isn’t necessarily more harmful than cane sugar.
"There is, however, no direct evidence for more serious metabolic consequences of high fructose corn syrup versus sucrose consumption." 
"The progressive replacement of sucrose by HFCS is however unlikely to be directly involved in the epidemy of metabolic disease, because HFCS appears to have basically the same metabolic effects as sucrose. " 
More studies will have to be conducted to conclusively state if HFCS is indeed worse than sucrose. Neither are good for you, of course, in excessive amounts. I suppose that meanwhile, to be on the safe side, you should reduce the intake of both.
“There is more goat meat eaten in the world than any other meat animal. 65 - 70% of all red meat eaten in the world is goat meat.
There is more goat milk consumed in the world than cow milk
The goat is the one of the oldest domesticated animals in the world”—
It really depends on what you mean by “night owl”. There is a condition that is called Delayed Sleep Phase Syndrome, which is a disorder that changes a person’s general sleep, peak period of alertness, and so on.
People with the disorder who try to live on a normal schedule cannot fall asleep at a “reasonable” hour and have extreme difficulty waking because their biological clocks are not in phase with that schedule.
This quote basically says that yes, quite certainly, when one with DSPS (that is, an extreme “night owl”), will have difficulty waking up in a morning, and wake up slower than an “early bird”, but only if they are being forced (by work or otherwise) to live on a schedule that their body doesn’t naturally want to do.
Imagine if a ‘regular’ person had to wake up every morning at 3am for their job. They would hit the snooze button just as much as one with DSPS does when they wake up at 8am.
If, however, they are allowed to follow their own schedules, e.g. sleeping from 4 a.m. to noon, they sleep soundly, awaken spontaneously, and do not experience excessive daytime sleepiness.
* italics not originally in text, and used to accentuate a point.
I will attest to the fact that, as someone with DSPS, when it’s time for me to wake, I will awaken instantly, and be ready for the day. I’m generally not sleepy for very long. That being said, it may be around 10:30 - 11:30, but when one sleeps at 2:30am - 3:30am that’s a full 8 hours of sleep.
So, I would have to say, in full confidence to the question “Do night owls wake up slower than early birds?”
Yes when they must wake up earlier than their normal waking time. No if they awaken on their own accord.
I know this is from “Science News for Kids,” but it reminded me of a talk I heard recently that included discussion of this research.
For every cell in your brain, bones, organs and blood, there are 10 bacteria. They’re not going anywhere, so you might as well get used to them.
Not new news, but still interesting to think about.
Even more interesting are the experiments showing that germ-free mice, never colonized with normal gut bacteria, engage in more exploratory behavior than their normally-colonized brethren. If young germ-free mice are then colonized, their behavior reverts to the norm. But it they’re not colonized until they’ve reached maturity, they remain “bold and adventurous.”
More evidence that what you eat influences the bacteria in your intestine, which in turn, affects your brain.
A landmark new study out of Texas confirms this, having found that not only do diet sodas not help with weight loss, but they actually cause both weight gain and health problems.
Researchers from the University of Texas Health Science Center (UTHSC) at San Antonio gathered ten years worth of data on 474 participants from a larger, ongoing study called the San Antonio Longitudinal Study of Aging. Among these participants, those that consumed two or more diet sodas a day experienced waist size increases that were a shocking six times greater than those who did not drink diet soda.
In a related study presented at the same time, researchers also found that aspartame, a commonly-used chemical sweetener in diet foods and beverages, is actually responsible for raising blood sugar levels.
US Food and Drug Administration adverse event reports going back several decades indicate that artificial sweeteners like aspartame are also responsible for destroying brain neurons, which in turn leads to a host of chronic illnesses.
These include, but are not limited to, chronic headaches, seizures, strokes, vascular disorders, heart disease, premature birth, dementia and other brain disorders, and cancer
So rather than consume artificially-sweetened beverages and foods with the hope that they will somehow induce weight gain and promote health — two notions that have proven once again to be false — the best way to begin to lose weight is to consume less processed, refined sugars and simple carbohydrates in the first place. Read the full article here.
This may not be what some of you want to hear, but it’s important that we all know the damaging effects of artificial, processed food and drink. Long-term weight loss isn’t just about “counting calories”.
RESULTS: SMRs for all causes of death were significantly below the reference level of 100 in both studies: 52 (95% confidence interval (CI) 49-56) based on 1,131 deaths in the Oxford Vegetarian Study and 59 (57-61) based on 2,346 deaths in the Health Food Shoppers Study. For all causes of death, the DRR for vegetarians compared with non-vegetarians was close to one in both studies: 1.01 (95% CI 0.89-1.14) in the Oxford Vegetarian Study, 1.03 (0.95-1.13) in the Health Food Shoppers Study. CONCLUSIONS: British vegetarians have low mortality compared with the general population. Their death rates are similar to those of comparable non-vegetarians, suggesting that much of this benefit may be attributed to non-dietary lifestyle factors such as a low prevalence of smoking and a generally high socio-economic status, or to aspects of the diet other than the avoidance of meat and fish.
Baking soda and cornstarch: Using baking soda as a deodorant is a simple way to combat body odor without subjecting your pits to a variety of chemicals. Mix an eighth of a teaspoon of baking soda with a little bit of water — don’t dissolve it — and rub it under your arms. You can also create a baking soda and cornstarch mix to fight odor and help prevent wetness. Simply mix one part baking soda with six parts cornstarch and dust a little on your underarms.
Lemon juice:The citric acid in lemon juice can kill odor-causing bacteria, and there are people who swear by the lemon deodorizing method.
Rubbing alcohol:Rubbing alcohol is another inexpensive and easy deodorant that kills odor-causing bacteria. Simply fill a spray bottle with alcohol and spritz your underarms with it. You can even add a few drops of your favorite essential oil to give it a scent — witch hazel absorbs oil and is mildly astringent, and tea tree oil can help relieve body odor.
You can also make some combination of the above, adding coconut oil, shea butter, cocoa butter, etc.
Good article. Main point is that your car’s interior surfaces release benzene into the air, so it’s smart to open your windows before turning on the AC if at all possible…
On a sunny day, the temperature in a parked car can be more than 40 degrees (Fahrenheit) higher than the outside air.
The National Institute for Occupational Safety and Health (NIOSH) has a limit for short-term (15 minute) workplace exposure (3.2 mg per cubic meter) and for average workday exposure ( 0.32 mg per cubic meter).
Several other studies — from Germany, South Korea, and the United States — have looked at benzene levels in moving cars. These levels have ranged from 0.013 to 0.560 mg per cubic meter
It’s impossible to know whether these guidelines for benzene levels are high or low, nor are you likely to get your car tested for interior benzene emissions.
Of course benzene is only one of many chemicals leached by your car’s interior.
The upshot is that it’s good to let in some fresh air when you first get in your car and to leave the windows if you can.