Science & Fun - Jonathan Graehl

From David Eagleman’s book

Sound and vision are integrated at a low level. Double-beep with single-flash is perceived as double-flash.

What gets sent to higher-level processing are differences between expected input and actual input (number of connections sending info from higher-level part to lower-level vision is greater than low->high). Also e.g. you can’t tickle yourself. [perhaps this anticipation helps learning precisely timed hand-eye (more generally: motor-sensory) moves as in sports, music, and dance]. Further, decisions, movements, and inputs are shifted (after learning) so that causally-connected inputs+decisions are perceived as happening at the same time (they’re not; different senses have different lags). e.g. if a button->flash mechanism has a 1/10 sec delay, you’ll adjust and feel that the light comes on at the same time as you push the button; remove the delay, and then on your next push you think the light came before the push.

More visually-salient events (a larger/brighter/moving square) are perceived as longer duration.

Implicit learning: e.g. unconscious (visual) learning: experts at sexing day old chickens, or spotting German vs. British planes in WWII, are clueless to describe the features they use. But after weeks of teaching by example (student gets the same view, guesses yes/no, is corrected by expert) most people can learn.

People who can’t recall any new memories learn the skill of Tetris exactly as well as normal people; their dreams are also filled with falling blocks, although they won’t remember that they came from a game they were playing.

Liking those who are like you: if Rasputin shares your birthday, you describe him in more favorable terms. If something or someone has a similar name, you like them more. Weird. Presumably there’s some innate same-physical-type (obviously including race, maybe sex) respect or liking as well. First-letter match of name matters for profession, mate, etc. and first-sound or first-few-letters is even stronger.

Priming/exposure: even though you don’t remember seeing something recently, you’re more likely to recall it (e.g. look at your word choices). If you’ve seen a face before, you’ll find it more attractive than if it’s new (stranger danger?) If you’ve heard a claim before (even if you judged it dubious or false the first time), you’re more likely to think it’s true the second time (possibly part of you remembers that it’s familiar and that’s weak evidence for its validity; this seems reasonable to me, and of course that vote can be overwhelmed if you remember specific strong reasons against it).

Association: standard advertising tricks.

Hunches: shuffled decks of cards with win/lose (money) outcomes; you know some are more favorable than others. You’ll take 25 draws before you’ll say which decks are good, but you have sweaty hands drawing from a bad deck by the 13th draw.

Soliciting hunch-feelings: if you’re not self-aware, flip a coin to decide. If, seeing the result, you think letting the coin decide is stupid, your hunch was for the opposite. If you go along with the coin, then you had no strong hunch to the contrary. That’s why telling someone “flip a coin to decide” after they’ve reached an impasse is useful advice (if they don’t follow it perfectly).

Brains of experts are faster and more energy efficient (in their expert skill, of course) than people who are worse. We can speculate that they were spending more energy while learning (and consciously coaching themselves, or listening to coaching). People who learned Tetris well exhibited this pattern (eventually: electrically quiet brain; skill burned into [low-level?] efficient brain circuits). This is why experts can sometimes choke under pressure; they start interfering by trying to consciously control what’s become implicit.

i like how he leans, and sometimes leaps up from his legs w/ hooks + uppercuts - whether because he was crouched down in his dodging already, or because he’s short and loves to deliver a powerful up-driving blow.

and his practiced defense-patterns - http://www.youtube.com/watch?v=uYZzMPsm6c4
i have to believe some of it is really that-fast reactions and predictions, not only planned moves

[In] a continuing study of elderly Mexican and European Americans. The result: Diet soda drinkers saw a 70% increase in waist circumference compared with non-drinkers over the course of a decade. People who drank more than two diet sodas a day saw a staggering 500% greater waist circumference compared to non-drinkers.

(474 people studied for a decade; usual correlation disclaimers - fat people might replace real soda w/ diet, etc. - but I believe it’s causal)

HT

[Dr. Ramachandran] posits two different reasoning modules located in the two different hemispheres. The left brain tries to fit the data to the theory to preserve a coherent internal narrative and prevent a person from jumping back and forth between conclusions upon each new data point. It is primarily an apologist, there to explain why any experience is exactly what its own theory would have predicted. The right brain is the seat of the second virtue. When it’s had enough of the left-brain’s confabulating, it initiates a … paradigm shift to a completely new narrative.

 

For some reason, squirting cold water into the left ear canal wakes up the revolutionary. Maybe the intense sensory input from an unexpected source makes the right hemisphere unusually aroused. Maybe distoring the balance sense causes the eyes to move rapidly, activating a latent system for inter-hemisphere co-ordination usually restricted to REM sleep³. In any case, a patient who has been denying paralysis for weeks or months will, upon having cold water placed in the ear, admit to paralysis, admit to having been paralyzed the past few weeks or months, and express bewilderment at having ever denied such an obvious fact. And then the effect wears off, and the patient not only denies the paralysis but denies ever having admitted to it.

via Yvain

One of the things that has always baffled me about psychedelics such as LSD, LSA or psilocybin (the active ingredient of “magic mushrooms”) is that their actions seem far too specific to be caused by a simple substance.

The effect I am referring to is that for some people and in some contexts, they cause what is often called a spiritual experience, i.e., experience that is deeply meaningful to the user and possibly long-term world-view (and behaviour) altering.

Look for example at this study

There’s also this active study which is the object of a 12 minute report available on Youtube

From my limited experience, and from what I observed in friends, I would say that psychedelics can be used to increase rationality, specifically by eliminating those sources of irrationality stemming from self-deception. They seem to allow the reexamination of deeply ingrained beliefs about the self and the world, that are beyond everyday reach.

via comment on Yvain’s piece

If activating the right hemisphere leads to the ability to overturn current beliefs, why does the patient go back to their old beliefs after the effects wear off?

Good objection. But those people are brain-damaged. Maybe in normal people the insight will stick. If you try it, videotape yourself, just in case you revert.

When this test is done to patients in a hospital, the patient is lying in bed on his back facing upward towards the ceiling. Ice cold water, 60 ml total, is introduced into one ear canal using a syringe. This is repeated in the other ear canal.

Ouch.

Chronic stress has long been linked with neurodegeneration. Scientists at the 

University of Southern California (USC) have now found a mechanism:chronic stress (physical or mental) causes overexpression of the RCAN1 gene, in turn leading to neurodegenerative disease.

The mechanism involves these steps:

1. Chronic overproduction of RCAN1 causes hyperphosphorylation of tau proteins in the brain. (In a healthy person, the RCAN1 gene helps cells cope with stress.)

2  Tau proteins stabilize microtubules, which are like scaffolding, used to build the brain’s neurons. Previous research has shown that when the tau protein binds too much phosphate (a process called hyperphosphorylation), it forms snarls that prevent the brain’s signals from effectively traveling.

3. These neurofibrillary tangles eventually choke the life out of neurons, killing off brain function a tiny piece at a time in what is outwardly recognized as degenerative brain disease.

The researchers suggests that overexpression of RCAN1 is also connected to Amyloid beta (overproduction of the Amyloid beta peptide), a competing theory of neurodegeneration.

Coffee protects against Alzheimer’s, in spite of its alertness-inducing caffeine. The fact that this condition (too much RCAN1) causes lesions in the brain doesn’t mean that RCAN1 is bad (it’s not;

The researchers have also shown a connection between too little RCAN1 production and Huntington’s disease.

), or that a little stress is bad (it’s not). But it does provide some confirmation of what was already pretty well known: chronic high stress levels are incredibly harmful to any animal’s health. I’d like to understand what’s meant by “stress” more precisely, as what I believe about it seems almost tautological.

(HT)

After ingestion, fructose is absorbed from the mid to distal small bowel and almost completely metabolised by the liver, independent of the hormone insulin. Unlike glucose, fructose does not stimulate insulin release. Metabolism of fructose depletes intracellular energy stores (ATP), and induces uric acid production.14

 The principal products of hepatic fructose metabolism are triglycerides, which are then released into the circulation.

While fructose is processed, conversion of glucose to glycogen (glycogenesis) in the liver is blocked. The reduction in glucose metabolism, in turn, causes insulin levels to rise so that glucose is taken up in alternative sites, such as muscle tissue. Such high insulin levels leads to compensatory insulin resistance in muscle tissue.14 This mechanism may explain how fructose has little acute effect on serum glucose levels, but importantly, impairs glycaemic control after long-term exposure to high doses. Further details of fructose physiology are presented elsewhere.14

Using animal studies, researchers have documented adverse metabolic effects of refined fructose consumption. Rodents fed on high fructose and sucrose diets, but not high glucose diets develop features of the metabolic syndrome, such as hyperinsulinaemia, hyperuricaemia and hypertriglyceridaemia.14

In contrast to animal data, links between fructose and adverse health outcomes have not been so convincingly demonstrated in humans, although longer exposure studies and higher doses of fructose (>200g/day or the equivalent of two cups of sugar) tend to produce clearer adverse health outcomes. For example, small intervention studies have shown that high doses of fructose provoke insulin resistance within one week,15 whereas smaller doses (14 Whilst 200g is greater than the average New Zealand daily intake (70g/day), variation in consumption means that a substantial proportion of New Zealanders are likely to ingest more than 100g/day. A rise in systolic blood pressure of 7mmHg was observed after intake of 200g of fructose per day for 14 days in a randomised trial (n=74).16 This study also found adverse effects on triglycerides, fasting insulin and metabolic syndrome outcomes. Other effects include modest weight gain in some short term studies.17 The health effects of long term, high dose exposure of fructose, which occurs in some subsets of the population have not been studied in experimental trials.

14. 
    Johnson RJ, Perez-Pozo SE, Sautin YY, et al. Hypothesis: Could Excessive Fructose Intake and Uric Acid Cause Type 2 Diabetes? Endocr Rev. 2009;30(1):96-116.
15. Havel P. Dietary Fructose: Implications for Dysregulation of Energy Homeostasis and Lipid/Carbohydrate Metabolism. Nutrition Reviews. 2005;63(5):133-57.
16. Perez-Pozo SE, Schold J, Nakagawa T, et al. Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: role of uric acid in the hypertensive response. Int J Obes. 2009.
17. Raben A, Vasilaras TH, Moller AC, et al. Sucrose compared with artificial sweeteners: different effects on ad libitum food intake and body weight after 10 wk of supplementation in overweight subjects. Am J Clin Nutr. 2002;76(4):721-9.

source

refined sucrose is half fructose. corn syrup is roughly half fructose. fruits have fructose and sucrose, but are less concentrated and at least have fiber and polyphenols to slow digestion.

More work needs to be done to show that small amounts of fructose (like those obtained by a diet including fruits but not much refined sugar or corn syrup) are harmful and should be reduced. Perhaps the harm is very small, or nonexistent. But for sure, large amounts are harmful and cause obesity, diabetes, high blood pressure, and heart disease.  It’s definitely above average to consume over 400g of sugar and thus over 200g of fructose, daily, but probably 1/3 of American teens+adults do (complete guess).

Animals seem to remember/learn more while moving. This would make sense if you were mapping new territory.

Rhythms in the brain that are associated with learning become stronger as the body moves faster, neurophysicists at the 

University of California, Los Angeles, have found.

The experiment was performed by measuring electrical signals from hundreds of mice neurons using microwires, the researchers said. Nearly a hundred gigabytes of data was collected every day.

Analysis of the data showed that the gamma rhythm, a fast signal that occurs while concentrating or learning, gradually grew stronger as the mice moved faster.

(of course the measured signal becoming stronger doesn’t actually prove an increased learning outcome, but I expect it nonetheless)

This reminds me of Seth Roberts’ claims that treadmill walking (which lacks much of the visual “I’m moving fast” stimulus) helps him memorize and learn.

When you drive a car, you get visual movement input with little physical movement stimulus (some vibration and acceleration, and a feeling, if you’re driving, of being in control). It seems less likely that driving a car while listening to an audiobook aids learning compared to not driving (at the least, there’s divided attention).

When you walk on a treadmill, you don’t have to pay attention, but you still get a little jiggling of the visual field.

It may be the visual part is irrelevant.

I never mapped out streets and places much until I began driving myself at age 20. I’d walk and bicycle but only on a few fixed routes. But there’s a simpler explanation for that than “motion->learning” (necessity).

Effects of chewing gum on cognitive function, mood and physiology in stressed and non-stressed volunteers.

RATIONALE:

Recent research suggests that chewing gum may improve aspects of cognitive function and mood. There is also evidence suggesting that chewing gum reduces stress. It is important, therefore, to examine these two areas and to determine whether contextual factors (chewing habit, type of gum, and personality) modify such effects.

OBJECTIVES:

The aims of the present study were: (i) to determine whether chewing gum improved mood and mental performance; (ii) to determine whether chewing gum had benefits in stressed individuals; and (iii) to determine whether chewing habit, type of gum and level of anxiety modified the effects of gum.

SUBJECTS AND METHODS:

A cross-over study involving 133 volunteers was carried out. Each volunteer carried out a test session when they were chewing gum and without gum, with order of gum conditions counterbalanced across subjects. Baseline sessions were conducted prior to each test session. Approximately half of the volunteers were tested in 75 dBA noise (the stress condition) and the rest in quiet. Volunteers were stratified on chewing habit and anxiety level. Approximately, half of the volunteers were given mint gum and half fruit gum. The volunteers rated their mood at the start and end of each session and had their heart rate monitored over the session. Saliva samples were taken to allow cortisol levels (good indicator of alertness and stress) to be assayed. During the session, volunteers carried out tasks measuring a range of cognitive functions (aspects of memory, selective and sustained attention, psychomotor speed and accuracy).

RESULTS:

Chewing gum was associated with greater alertness and a more positive mood. Reaction times were quicker in the gum condition, and this effect became bigger as the task became more difficult. Chewing gum also improved selective and sustained attention. Heart rate and cortisol levels were higher when chewing which confirms the alerting effect of chewing gum.

CONCLUSIONS:

Overall, the results suggest that chewing gum produces a number of benefits that are generally observed and not context-dependent. In contrast to some previous research, chewing gum failed to improve memory. Further research is now required to increase our knowledge of the behavioral effects of chewing gum and to identify the underlying mechanisms.

via Effects of chewing gum on cognitive function, mood… [Nutr Neurosci. 2010] – PubMed result.

Maybe cortisol goes up with any physical activity.

Chewing gum might be bad for you in other ways (e.g. possible jaw RSI).

The improved focus and mood works under the quiet or the distressingly-loud-noise condition.

HT

During an average 11 years of follow-up, 28,851 deaths were identified. In Cox proportional hazards models controlling for tobacco use and other potential confounders, no associations were found between multivitamin use and mortality from all causes

(for users vs. nonusers:

hazard ratio = 1.07, 95% confidence interval: 0.96, 1.19 for men;

hazard ratio = 0.96, 95% confidence interval: 0.85, 1.09 for women), cardiovascular diseases, or cancer. The findings did not vary across subgroups by ethnicity, age, body mass index, preexisting illness, single vitamin/mineral supplement use, hormone replacement therapy use, and smoking status.

-study

The 1.07 hazard ratio (7% higher chance of dropping dead at any moment) for men is indeed not significant; a simpler model that doesn’t control for as many things (including use of some single supplement e.g. selenium) gives a HR=.99, for example.

It’s unlikely that vitamins do nothing. Yet they appear to, in this fairly large study of old people. I’d say this is reason to look at fine-tuning vitamin/mineral intake. Those men who took 1-6/week instead of 1x or 2x/day seemed to fare slightly better than 0/week (TOTALLY not significant though).

Too much of some things in diet+multivitamin is likely quite harmful to health. If you ignore statistical significance, the weak evidence is that those old people who take multivitamins for a 5 year stretch are slightly more likely to end up dead 10-15 years later.

Or, supposing that multivitamins aren’t harmful (they obviously vary tremendously in composition), it’s really true that it’s unlikely that your normal diet is lacking anything you need, and the non-significant effect is mostly due to confounds like taking vitamins because you feel your health start to fail, or taking vitamins because you live a healthy lifestyle already, etc.

Unfortunately, that multivitamins do nothing, or are both helpful and harmful, with the harms slightly outweighing the benefits, is the simplest explanation of many such null results in the literature. But I don’t want to accept it, because I know of some specific causal evidence suggesting that individual vitamins, when supplemented, yield health benefits in a majority of people. So I’ll hold the slightly more complicated: “most multivitamins are too-highly dosing at least a few things, in a way that harms health as much as the rest of it benefits health”, tentatively.

Another nearly siginificant pattern: people who’ve used vitamins for at least 5 years die less than those who recently started or never used (but again, not really significant). Motivated speculation (not wanting to believe multi-vitamins are actually net-harmful or -useless): old people who suddenly start taking multivitamins did so due to correctly feeling their declining health and imminent death. So their higher rate of death shouldn’t be blamed on having recently started multivitamins.

Best to worst:

Normal:
Farewell, Tell No One, The Way Back, Valkyrie, Twilight Samurai, Girlfriend Experience, Restrepo, Adjustment Bureau, Easy A

Horror/gross:
I Saw the Devil, Memories of a Murder, Tale of Two Sisters, Hard Candy, Serbian Film, Irreversible, Antichrist, Caged, Human Centipede, I Spit on Your Grave

Study:

(sadly: of insects, not humans. humans take too long to die?)

Most animals will keep eating until they have enough protein. In some insects, they’ll eat up to the level that shortens their lifespan but increases their reproductive output.

increasing the ratio of protein and non-protein energy in the diet decreases lifespan; but as seen in the example from male crickets discussed above, if this ratio falls too far there is an increased risk of decreased longevity associated with obesity

uh-oh. i like my high-protein diet. i need muscles to do well in soccer and volleyball. and it’s easy not to overeat when you’re not craving protein. this suggests a benefit from titrating protein somehow (being sensitive to how much of it you need for your activity level).

protein intake is more strongly regulated than that of carbohydrate and fat [20]. As a result, protein appetite drives overconsumption of energy on low percent protein diets, promoting obesity and metabolic disorders with consequent effects on longevity

so, be skinny, on as little protein as you can get away with (obviously you’ll die with 0 protein in your diet; likewise with 0 fat).

the major causes of increased longevity in studies on calorically restricted primates (most recently [30]) is a reduction in the incidence of diabetes, cancer and cardiovascular disease relative to ad libitum fed controls. This may not result from benefits associated with CR per se, but rather reflect the costs of nutrient imbalance when feeding ad libitum on a fixed diet. As the required balance of nutrients changes over time (with time of day, season, growth and development, and senescence), animals will be forced to overeat some nutrients to gain enough of others

speculation without evidence - they seem to be suggesting that ideally you eat the minimum amount of food necessary for all vitamin / macronutrient needs. but it’s also true that if you have excess body fat, you’ll survive surgery better. some excess makes you more robust. we can’t really titrate perfectly.

i suppose the overall question would be: how much quality of life do you have to sacrifice by risking insufficient intake of various nutrients, in order to maybe live longer? nobody knows the answer for humans, yet.

When protein is eaten in higher then optimal quantities relative to non-protein energy it shortens lifespan - in insects certainly and perhaps too in mammals

yes, perhaps. i hope not, but it needs to be studied - how sensitive is the curve? how “too much” can you do while barely reducing lifespan?

- but what might the underlying mechanisms be? There are several possibilities, including enhanced production of mitochondrial radical oxygen species [19,31], DNA and protein oxidative modification, changes in membrane fatty acid composition and mitochondrial metabolism [19,32], changes in the relationship between insulin/IGF and amino acid signaling pathways, including TOR [33-38], toxic effects of nitrogenous breakdown products and capacity to deal with other dietary toxins [39,40], changes in immune function to pathogen attack [41,42], and changed functioning of circadian systems [43].

(their hypothesis … AMPK extends life unless you have too much and develop metabolic syndrome (the obesity disease), TOR shortens it.)

insects are quite different than humans. i’m waiting for more evidence that a high-protein-ratio diet shortens life (but i’ve suspected/feared it for a while)

Phytic acid isn’t well understood (at least, its impact on human health isn’t), but it’s definitely found in many nuts and grains (white flour and rice have far less of it; it’s mostly in the hulls/bran), and is good at removing minerals (by chelation) from the human body, e.g. zinc and iron, which is generally bad. On the other hand, it’s nice for removing uranium from the body. It also reduces colon cancer. It penetrates the brain and can protect neurons there by chelating iron (which I guess you don’t want in the brain - iron does get in there somehow and exacerbates many brain diseases).

Grain consumption has long been known to damage vitamin D status and bone health. Indeed, it is difficult to induce bone frailty in laboratory animals without feeding them grain. In Edward Mellanby’s original experiments leading to the discovery of vitamin D, he induced rickets by feeding dogs a diet of oats or wheat bread. [3] In human infants, wheat bran induces rickets. [4] In addition to interfering with vitamin D, grains also contain high levels of phytic acid, which interferes with bone mineralization by blocking absorption of calcium and magnesium.

source (while making fun of Gwyneth Paltrow’s ridiculous macrobiotic diet)

Another crucial factor in bone health is vitamin K2. Since dairy fats are the leading source of vitamin K2, it’s likely Ms. Paltrow was deficient in this crucial vitamin. Most people are deficient in vitamin K2 – let alone those who avoid meats and dairy.  In clinical trials, vitamin K2 supplementation reduced non-vertebral fractures by a remarkable 81%. [5]

reduced by 81% = 1/5 the odds. I like milk. Funny that they thought it was calcium (with supplemented D to aid absorption) that made milk bone-friendly, since it’s pretty easy to get enough calcium in general.

a high omega-6 to omega-3 ratio reduces bone density.

omega-6 = vegetable oil (roughly - saturated vegetable oils obviously aren’t), omega-3 = fatty cold water fish

The fact that paleo people get excited about phytic acid shows that they’re looking for confirmation of their already-held beliefs (grain is bad! etc.)

Fermentation, cooking, and sprouting whole grains, significantly reduce phytic acid content. Almonds and sesame seeds are very high in it; toasting them might help.

It seems like you can benefit from moderate phytic acid (nullifying iron in your brain sounds good), by simply ensuring you have excess of the minerals it chelates and steals from you.

source: http://perfecthealthdiet.com/?p=1177

You need DHA in your diet (EPA can be synthesized from ALA, which is in flaxseed oil; DHA barely can). But high levels of polyunsaturated fats may be dangerous; they’re easily oxidized (anecdotal evidence; natural diets don’t have high levels, unless they’re mostly fish):

You can supplement DHA from some particular type of seaweed (I forget the details), or in many fatty fish or their extracted oil (watch your mercury). It does occur naturally in lesser quantities in various other foods. DHA lowers testosterone, but it has many good effects. Lower testosterone means more (harmless, operable) prostate cancer, but possibly more frequent severe cases:

if DHA is dangerous, low-fat dieters will be in the most trouble. Another reason to eat a high-fat diet.

(the ratio matters; eat more saturated fat to mitigate the harms while still getting some of the benefits of DHA)

Most Americans eat far too much omega-6, and their omega-6 to omega-3 tissue ratio is too high, which is pro-inflammatory via the COX-2 pathway. Eating omega-3s including DHA reduces inflammation by downregulating the COX-2 pathway. This accounts for the well-attested benefits of DHA against cardiovascular disease. Now, cancer is promoted by COX-2 pathway inflammation, which is why COX-2 inhibitors such as aspirin and ibuprofen are protective against cancer. [4] DHA’s action to downregulate this pathway must generate an anti-cancer effect. But, unlike aspirin and ibuprofen, DHA has no observable effect on overall cancer risk. This suggests that DHA has other effects, unrelated to its anti-inflammatory activity, that are cancer promoting. These counterbalance the benefits from its anti-inflammatory effect. If DHA has pro-angiogenic effects that are independent of COX-2 mediated inflammation, then this could account for the observations.

One reason an association of DHA with high-grade cancer may have been missed is that it would be detected only in large studies able to segregate cancers by grade.

 

 a person in whom the immune system is trying but failing to clear elevated CEP levels almost invariably has macular degeneration (AMD)

AMD = why 1/3 of people 75+ yr old are nearly blind. DHA is the only cause of CEP. It’s caused by excessive growth of blood vessels dislodging the retina. DHA is concentrated near the retina (is 80% of the PUFA in it). Photons cause oxidation, and DHA is extremely oxidizable. Antioxidants help slow AMD. Finally, adding CEP directly to mice causes AMD (this was shown in 2003). (we know now it’s because CEP causes angiogensis).

CEP is normally good. It brings immune cells from bone marrow to the wound. Cancers and AMD give chronic CEP elevation. CEP actually causes wound healing even in mice with normal wound healing mechanisms crippled (VEGF and TLR2 knocked-out or inhibited) - this was shown in 2010. VEGF causes angiogenesis when tissue is oxygen deprived. TLR2 causes angiogenesis when it detects oxidative stress.

vitamin A + DHA yield CEP (via retinyl from A + HOHA=oxidized DHA).

If you’re going to take DHA (usually fish oil) you’ll want anti-oxidants. Oxidation can’t be avoided; it’s essential to metabolism and fighting infection.

At the moment, I think it’s prudent to eat no more than 1 pound of salmon or similar cold-water fish per week, to avoid further EPA/DHA supplements, and to avoid low-fat diets which tend to elevate membrane DHA levels. Moderate omega-3 consumption is especially important for those suffering from diseases of pathological angiogenesis – especially cancer. DHA is essential for good health – but in excess, it is probably dangerous.

ouch.

DHA + retinyl + oxidative stress = angiogenesis

This recipe is invoked normally and properly during wound healing. But it is also invoked excessively in pathological contexts – notably in cancers and age-related macular degeneration, probably also in other angiogenesis-associated diseases such as arthritis, rosacea, obesity, psoriasis, endometriosis, dementia, and multiple sclerosis.

 Finasteride raises DHA levels, and DHA lowers testosterone. Low testosterone reduces incidence of low-grade prostate cancers but makes it much more likely they will progress to high-grade. Thus, finasteride reduces prostate cancer incidence but increases high-grade prostate cancer incidence and overall prostate cancer mortality. Fits all the facts. Could be.

source: http://perfecthealthdiet.com/?cat=27

My bottom line: the Brasky study is weak evidence for anything, but it does raise a whiff of evidence that high dietary fish oil intake might encourage a transition from low-grade to high-grade cancer.

Lycopene may be the most powerful carotenoid quencher of singlet oxygen,[18] being 100 times more efficient in test tube studies of singlet-oxygen quenching action thanvitamin E … The absence of the beta-ionone ring structure for lycopene increases its antioxidant action….

Lycopene is not modified to vitamin A in the body …

So lycopene does not increase retinyl levels, but does act as an extraordinarily powerful antioxidant, thus reducing oxidative stress! If you wanted a good food for stopping the DHA – angiogenesis pathway, you’ve found it: tomatoes.

Eat tomatoes. (the other carotenoids mostly can convert to vit A, and overly high levels of vit A mean slightly higher risk of aggressive cancer).

Prostate cancer is associated with low tissue levels of zinc. [7, 8] High dietary intake of zinc is associated with lower rates of prostate cancer. [9]

N-acetylcysteine is an antioxidant supplement that is a precursor to glutathione. N-acetylcysteine has been shown to prevent angiogenesis and has been proposed as a likely cancer preventative, but this is as yet untested. [10]

 Observational studies weakly link high DHA, high vitamin A, and low antioxidant status to diseases of angiogenesis such as cancer.

This pattern would be consistent with the idea that the natural pathway used in wound healing to trigger angiogenesis – DHA oxidation and combination with retinyl protein to trigger TLR-2 pathways – is also important for cancer progression.

It suggests a strategy of reduced fish oil and vitamin A consumption and increased intake of certain antioxidants (such as lycopene, zinc, selenium, or NAC) may be helpful against cancer.

However, this idea needs testing. No study in animal cancer models has tested this dietary combination.

Given the many proven benefits of moderate amounts of fish oil, I don’t see a reason yet to alter our recommendation that healthy people should eat a pound of fish per week. That said, I do think very high intakes of fish or fish oil are ill advised. And I’m intrigued by the idea that dietary changes may have the potential to play a powerful role in recovery from diseases of angiogenesis such as cancer.

A few years ago I started taking a high dose of Omega 3, because of joint inflammation, and other issues. This made big difference for about 3 months, then seemed to not work any more. I talked to a nutritionist friend and she pointed out that according to Andrew Stoll (The Omega 3 Connection) you must take 1000 mg vit C and 500 iu vit E daily or the omega 3 becomes oxidised in your body (cell membranes) and ineffective. I started taking both and in days was back to the original anti-inflammatory effectiveness of omega 3. I have since talked to others about this – for example a psychiatrist whose clients did well on omega 3 for 3 months and then it became ineffective.

quite anecdotal - needs actual research. but the fact that omega-3 are easily oxidized means they might degrade vit-C (which means you need enough carbs+selenium in your diet to move the DHAA out of the bloodstream into cells for reconversion to C, or you just need to bear the harm of DHAA and supplement more C. In general, vit E supplementation is quite harmful. I wouldn’t do it unless strong evidence revealed that it’s okay when you have high omega-3 intake.

Vitamin C deficiency tends to develop slowly over months, losing a little every day, so it’s quite plausible that a deficiency could develop over 3 months and lead to those changes in omega-3 oxidation.

It is possible that extra lipid peroxidation on a high-PUFA diet could help deplete vitamin C faster.

 

data seem to show that people taking particularly high doses of vitamin E (500 IU to 2000 IU) may have a slightly increased risk of death. However, taking 400 IU vitamin E per day did not increase the risk of death in a total of 15,000 patients studied in several different clinical trials.

source: http://www.nei.nih.gov/news/statements/vitamine.asp

Eating omega-3 fats promotes calcium oxalate kidney stones about as much as eating oxalate. The top quintile of dietary oxalate intake has a relative risk of 1.22. [12]  (The top dietary source of oxalate is spinach, by the way.)

a reminder from my last post:

Zero-carb dieters are at risk for

• Excess renal oxalate from failure to recycle vitamin C;
• Excess renal uric acid from disposal of nitrogen products of gluconeogenesis and ketogenesis;
• Salt and other electrolyte deficiencies from excretion of oxalate, urea and uric acid; and
• Dehydration.

 

If you feed lab animals high doses of polyunsaturated fat (either omega-6 or omega-3 will do) along with high doses of either fructose or alcohol, then fatty liver disease develops along with metabolic syndrome. Metabolic syndrome is a major risk factor for obesity, and it’s not very difficult to induce obesity on these diets.

source: http://perfecthealthdiet.com/?p=1963

Both sugar and vegetable oils are individually risks for obesity:

• Stephan did a nice post a few years back, “Vegetable Oil and Weight Gain,” discussing a couple of studies showing that both rats and humans get fatter the more polyunsaturated fat they eat.
• Dr. Richard Johnson and colleagues did a review of the evidence for sugar (fructose) as a cause of obesity in the American Journal of Clinical Nutrition a few years ago. [1]

What the animal studies show us is that when fructose and vegetable oils are consumed together, they multiply each other’s obesity-inducing effects.

Consistent with this, the obesity explosion in the UK and US is accompanied with dramatic increases (+200% or more) in both polyunsaturated fat and sugar (which is half fructose; roughly the same as high-fructose corn syrup, really).

PUFA (in many vegetable oils) is generally bad even though EPA+DHA are good.

Omega-6 PUFA intake is generally too high in our diet already. When you’re losing fat weight, you’ll have a lot of omega-6 in your bloodstream assuming you had a normal diet when you put it on, so that means you’d want even less omega-6 in your diet and more omega-3.

In the China Study, the correlation of wheat consumption with BMI was 56%, whereas the correlation of total calorie intake with BMI was only 13%. (Since total calorie intake is correlated with muscle mass, total calorie intake may be completely uncorrelated with fat mass. It’s not how much you eat, but how much wheat!)

Similar outcomes occur in mice. I can’t find any mouse studies comparing wheat to rice, but I did find one comparing wheat to rye [4]. Wheat was far more obesity-inducing than rye:

 

Since rye has gluten, it’s not just the gluten in wheat causing obesity (many people vilify gluten, but other than for a minority of people with celiac disease, it’s not clear what the problem with it is).

Dietary glucose is not likely to do much damage unless the body’s glucose-disposal machinery has been damaged by other toxins first.

(fructose is a toxin; something in wheat is a toxin); but fructose in a low-carb diet may go straight to glycogen (especially if it’s after exercise which drains your muscles’ glycogen stores), which is safe. fructose+saturated fat is safer than fructose+PUFA as mentioned above (thank goodness for all that saturated fat in my oversweetened ice cream!)

It’s possible, by the way, that differing toxicities among grains could be responsible for epidemiological evidence favoring “whole grains” over “refined grains.” In America, products made with refined grains are usually 100% wheat; but products made with whole grains are often of mixed origin (“7 grain bread”). Since wheat is the most obesity-inducing grain, dilution of wheat content may be masking the toxicity of whole grains.

 

 I also eat bananas and stone fruits and tend to avoid apples and pears.

(apple+pear are essentially fructose+fiber. fiber may slightly reduce the harm from fructose, but it’s still bad)

Beans have a lot of toxins in their raw state. They can sometimes be detoxified by overnight soaking and thorough cooking. With commercial products we don’t really know what they did to process the beans.

I really do think commercial beans are soaked and cooked.

There isn’t an obvious minimum required amount of carbs in the human diet.

However, a diet too low in carb+protein calories is definitely bad.

Further, when fighting infection, it’s tricky to give your body what it needs if you’re not getting enough carbs. Without enough (protein or carbs) you won’t get the insulin needed to recycle oxidized vitamin c produced when fighting infection (you can supplement C, but the unrecycled oxidized byproduct is itself harmful). If you must have a near-0-carb diet, you should supplement with NAC, selenium, zinc, copper, coenzyme Q10, ALA, and colorful veggies/berries, especially if fighting infection.

It’s almost impossible to make animals carb-deficient; they have large livers (which manufacture glucose) relative to their small brains’ glucose needs.

Glucose is needed for immune function and mucus.

If your mucus is low enough, you’ll get far more constipation and gut cancers, as do people who’ve followed the “Optimal Diet” popular in Poland. The reason ulcers and stomach cancers are greatly increased with Helicobacter pylori bacterial infection is that the stomach mucus is severely reduced:

You’ll get 100x more kidney stones on an extremely low-carb diet unless you specifically mitigate several factors.

If you’re mucus-deficient enough, you’ll have dry, bloodshot eyes and dry mouth. If that happens, you definitely need more glucose (meaning more protein possibly, but the simplest solution is to add slightly more carbs). White rice is a safe source of carbs.

source: http://perfecthealthdiet.com/?p=1032

Zero-carb dieters are at risk for

• Excess renal oxalate from failure to recycle vitamin C;
• Excess renal uric acid from disposal of nitrogen products of gluconeogenesis and ketogenesis;
• Salt and other electrolyte deficiencies from excretion of oxalate, urea and uric acid; and
• Dehydration.

These four conditions dramatically elevate the risk of kidney stones.

To remedy these deficiencies, we recommend that everyone who fasts or who follows a zero-carb diet obtain dietary and supplemental antioxidants, eat salt and other electrolytes, and drink lots of water.

Also, unless there is a therapeutic reason to restrict carbohydrates, it is best to obtain about 20% of calories from carbs in order to relieve the need to manufacture glucose and ketones from protein. This will substantially reduce uric acid excretion. If it also reduces vitamin C degradation rates, as we argued in 

our last post, then it will substantially reduce oxalate excretion as well.

The argument that carbs (or at least insulin, which you can get by eating a lot of protein also) help clear out degraded vitamin C is partially anecdotal, but seems reasonable to me:

• An infection or some other stress (e.g. injury, cancer) leads to the oxidation of extracellular vitamin C; and
• On a low-insulin or glutathione-deficiency-inducing diet, oxidized vitamin C is not recycled.

The immune response to infections generates reactive oxygen species, which oxidize vitamin C. Oxidation removes a hydrogen atom from vitamin C, turning it into “dehydroascorbic acid,” or DHAA. If DHAA remains in the blood, it degrades with a half-life of 6 minutes. [3]

Infections can cause vitamin C deficiency on any diet. During the “acute phase response” to infection or injury, vitamin C often becomes deficient. Here is a nice paper in which French doctors surveyed their hospital patients for scurvy:

We determined serum ascorbic acid level (SAAL) and searched for clinical and biological signs of scurvy in 184 patients hospitalized during a 2-month period.

RESULTS: The prevalence of hypovitaminosis C (depletion: SAAL

So half were at least depleted in vitamin C and 17% had outright deficiency, which if it persisted would produce scurvy.

DHAA can be recycled back into vitamin C, but only inside cells.

DHAA transport is crucial for brain vitamin C status. There is no direct transport of vitamin C into the brain, yet the brain is one of the most vitamin C-dependent tissues in the body.

Supplying DHAA to stroke victims (of the mouse persuasion) as late as 3 hours after the stroke can reduce the stroke-damaged volume by up to 95%:

DHA (250 mg/kg or 500 mg/kg) administered at 3 h postischemia reduced infarct volume by 6- to 9-fold, to only 5% with the highest DHA dose (P

Once inside the cell, DHAA is recycled back to ascorbate, mainly by glutathione inside mitochondria

Glutathione is recycled mainly by an enzyme built with selenium. Zero-carb diets deplete selenium levels. Once that happens, you’ll have a Glutathione deficiency. (NAC is a Glutathione precursor, thus the recommendation to supplement if low-carb, especially if ill. You can also directly supplement Glutathione, taken with lots of water and no food).

source: http://perfecthealthdiet.com/?p=1139

Vitamin C supplementation while ill makes sense, but you definitely want to have enough insulin and glutathione to recyle it to avoid the damage its “used” version creates:

In 1970, I discovered that the sicker a patient was, the more ascorbic acid he would tolerate by mouth before diarrhea was produced. At least 80% of adult patients will tolerate 10 to 15 grams of ascorbic acid … The astonishing finding was that all patients … can take greater amounts of the substance orally without having diarrhea when ill or under stress. [5]

Extremely high dose intravenous vitamin C is effective in some cases.

The patient tries to TITRATE between that amount which begins to make him feel better and that amount which almost but not quite causes diarrhea. [5]

Recall that in animals, vitamin C synthesis rises as much as 100-fold under disease. In humans, the limit of bowel tolerance rises up to 20-fold during illness. This suggests that bowel tolerance limit is an indicator of need.

Maybe. Bowel tolerance may be well over the optimum. But if it’s too hard to predict the optimum, it may be better than some fixed, modest amount.

 it is my experience that ascorbate has little effect on the primary fungal infections

Well-nourished humans usually contain not much more than 5 grams of vitamin C in their bodies….

If a disease is toxic enough to allow for the person’s potential consumption of 100 grams of vitamin C, imagine what that disease must be doing to that possible 5 grams of ascorbate stored in the body. A condition of ACUTE INDUCED SCURVY is rapidly induced.

Nah. Maybe the 100g tolerated is quickly pissed/shit out. But say only 90% of it is wasted excess - then his point still carries weight.

Speculation: it’s possible that Vit C is useful/protective against the poisonous ROS byproducts of the immune response, at a rate that exceeds the maximum recycling bandwidth via whatever (insulin+glutathione) is available. In that case, maybe the harm of the degraded Vit C is worth bearing.

Conventional wisdom is correct in that only small amounts of vitamin C are necessary for this [antioxidant] function because of its [recycling and] repeated use. The point missed is that the limiting part in nonenzymatic free radical scavenging is the rate at which extra high-energy electrons are provided through NADH to re-reduce the vitamin C and other free radical scavengers. When ill, free radicals are formed at a rate faster than the high-energy electrons are made available. Doses of vitamin C as large as 1-10 g per 24 h do only limited good. However, when ascorbate is used in massive amounts, such as 30-200+ g per 24 h, these amounts directly provide the electrons necessary to quench the free radicals of almost any inflammation. Additionally, in high concentrations ascorbate reduces NAD(P)H and therefore can provide the high-energy electrons necessary to reduce the molecular oxygen used in the respiratory burst of phagocytes. In these functions, the ascorbate part is mostly wasted but the necessary high-energy electrons are provided in large amounts.

I guess my speculation above is right.

Another early view was that vitamin C helps by destroying histamine, which may be produced in excess under conditions of stress.

“early view”? sounds like it’s not a good view :)

the oxidized form of vitamin C, dehydroascorbate, has strong antiviral activity in vitro.

DHAA is the (harmful) used vit-C byproduct that’s normally recycled.

 in clinical experience, vitamin C is most effective against viral infections.

Since animals upregulate ascorbate production under all kinds of stress, not just viral infections, it seems probable that vitamin C aids health by multiple pathways, not only by antiviral activity.

Vitamin C is extremely safe. Intravenous doses of 120 g/day given to cancer patients have been well tolerated.

In animals such as chickens that lack the ability to synthesize vitamin C, vitamin C is recognized as a means of supporting bacterial and viral immunity.

A well-tested therapeutic strategy would be to take 4 g vitamin C every hour with water until bowel intolerance is reached. The therapy is extremely safe, and its effectiveness is usually apparent within days.

Supposedly low iodine and D are common with prolonged infections. Maybe selenium (may just be in case of low-carb). Meat has plenty of selenium, of course.

Daily supplementation with high vit-C while not ill has some preliminary contraindicative research. Over-supplementing with vitamin E (fat soluble and toxic) is definitely bad. C might be ok.

(a) The Ristow paper administered vitamin E along with the C, see below for issues with that.

(b) Suppression of glutathione peroxidase and zinc-copper superoxide dismutase levels by C supplementation could be dependent upon levels of selenium and copper intake; so far only a small part of “supplement space” has been explored. What would be the effect of co-supplementation of C with selenium and copper?

(c) I can easily believe that vitamin C reduces the stress of exercise, but why isn’t the response to that more intense exercise, rather than elimination of vitamin C? Isn’t better tolerance of exercise a benefit for athletic training?

I’m not denigrating these papers, there could be reasons to avoid routine gram doses of C. But it needs more research. The benefits of C at 500 mg to 1 g/day in healthy people are more well established than these possible harms.

(2) The higher death rates are mainly in trials with vitamin E, sometimes beta carotene, both of which raise death rates on their own. When vitamin C is trialled on its own, the results have been mixed, but on my reading net positive.

In the case of C, our advice is more precautionary. Deficiency is tremendously harmful, but excess is virtually harmless. In trials, the benefit may be non-existent for 95%, but 5% may see big benefits and 0% harm. In trials the 95% dilute the benefits to the 5% out of statistical significance. Since the greatest benefit is likely to come in preventing infections from taking root, and everyone gets exposed to pathogens from time to time, we can’t know which of the 100% will benefit from the supplementation. So it makes sense to take a prophylactic supplement.

E and beta carotene seem to do damage. C and glutathione are essentially similar in status, C recycles glutathione and glutathione recycles C, so supplementing C is the most straightforward way to improve glutathione status. I happen to think glutathione is extremely beneficial and this is part of the reason I support C supplementation.

I do think you need a balance of the natural antioxidants, which is why copper and zinc (for zinc-copper superoxide dismutase) and selenium (for glutathione peroxidase) supplementation, and avoiding iron deficiency (for catalase), are important along with C supplementation.

We recommend obtaining vitamin E from foods only. If supplements are taken, they should supply low doses of mixed tocopherols and tocotrienols, not alpha-tocopherol only.

NAC we recommend for treating infections, not otherwise.

(NAC is popular in bodybuilding supplements, most of which do nothing to grow muscle - the legal ones, at least)

C and selenium and a good diet, NAC in infections, should be sufficient to make liver glutathione.

Plant antioxidants I would avoid. I think the natural, mitochondrial antioxidants are going to be more beneficial than food antioxidants that don’t penetrate mitochondria (where antioxidants are most needed) and that suppress ROS signaling.

weird. C is a plant antioxidant. carotenoids also (-> vit A) which give healthy (yellow-orange) looking skin and help immune function and neuron function. He must mean some other plant antioxidants (either tocopherols (vitamin-E like), polyphenolics (e.g. in balck tea, raspberries), or terpenoids (aromatic oils - citral, menthol, camphor, cannabinoids)?)

source: http://perfecthealthdiet.com/?p=636

 

Unsolved cipher-taunt thought to be from the Zodiac Killer:

(http://www.zodiackiller.com/340Cipher.html)

http://www.opordanalytical.com/articles1/zodiac-340.htm
hilarious

also hilarious

huh?

(source)

FBI effort (attached) - starts out looking good, then the language model takes over and it seems nearly as laughable

 

 

Ignoring the superstitious pseudo-evolutionary constellation of beliefs associated with it, I think “paleo” believers are doing a good job noticing severe flaws in conventional diet and health advice. The main dietary themes seem to me: plenty of protein is good, saturated animal fat is good, non-contaminated fish are good, colorful vegetables are good, high carbs (as far as it causes high insulin or appetite) is bad, fructose is bad (oddly, they usually recommend fruits anyway, especially berries), nuts+avocados are good, grains are bad (they’re divided on that; some people legitimately suffer from grains - tubers/squashes instead), full-fat and/or fermented dairy is better than low-fat (also divided; over half the world is lactose intolerant, so non-fermented dairy would be a bad idea for them), and, in terms of supplementation: plenty of DHA (fish oil) and vitamin D (sunlight or pills), otherwise RDA plus a little.

It’s very easy to induce obesity in both animals and humans: feed a malnourishing diet providing calories in the form of a combination of wheat, fructose, and polyunsaturated fats.

- http://perfecthealthdiet.com/
(presumably he means omega-6 polyunsaturated fats, and not EPA/DHA (omega-3))

An interesting paleo dissent (in favor of high-carb, low-fat, low-meat eating). Probably healthy enough but it won’t support intense physical activity.

Some smart folks have noticed that you have at least initial success with low-food-reward calorie consumption (basically: don’t combine a source of calories with something that’s fun to eat). e.g. Seth Roberts

This guy dissents:

• I think the focus should be on recovering health by curing metabolic damage.
• I think our evolved preference for tasty foods including starches, fat, salt, and other “high reward” flavors indicates they are healthy, and therefore that a diet rich in such foods is most likely to cure metabolic damage.
• I think it is essential to stay away from toxic, malnourishing foods made from wheat, fructose sugars, omega-6 oils, and bioactive compounds like MSG; and instead to eat foods that accord with our evolutionary history.

By metabolic damage, he means one of many possible things that can go wrong, with fat cells, the brain, hormones, whatever (really yet to be completely discovered). He objects to focusing on food-reward because he thinks that the fact that low-reward diets’ initial effectiveness is almost never sustained. By the way, the concept of “metabolic damage” being responsible for obesity is controversial amongst the “fat people have no willpower” crowd, but clearly diabetes fits the description.

Don’t supplement with too much calcium. Not only does high calcium prevent bone turnover (which you want), but it prevents magnesium absorption (oddly enough, supplementing magnesium will also help calcium reach bones).

high calcium intake can reduce the enlargement of the appendicular bones that generally occurs with ageing as a mechanical compensation for a decline in bone mineral density. Furthermore, high calcium doses slow bone turnover and also reduce the number of active bone remodelling sites. This situation can lead to a delay of bone repair caused by fatigue, and thus increase the risk of fractures independent of bone mineral density.

The highest quintile of calcium intake did not further reduce the risk of fractures of any type, or of osteoporosis, but was associated with a higher rate of hip fracture, hazard ratio 1.19 (1.06 to 1.32).

20% higher risk! Huge. A U-shaped dose/response curve is common in most vitamins (except those that can be pissed out easily, mostly water soluble like Vit B)

 - Dietary calcium intake and risk of fracture and osteoporosis: prospective longitudinal cohort study.

(HT)

Also:

Most people probably get insufficient amounts of dietary magnesium, but it’s one of the most important minerals for overall general health, including the stress response system. It’s nigh impossible to overdose (you’ll just have to hit the toilet), making it very safe to supplement – so do it! Take some magnesium if you aren’t eating leafy greens and nuts on a regular basis.

Excessive cortisol is the bad guy, obviously, and black tea has been shown to reduce stress, lower stress-induced cortisol, and increase relaxation when compared to placebo.

L-Theanine, which is present in green tea leaves, has anti-stress properties, most likely by inhibiting cortical neuron excitation. This goes for both psychosocial and physiological sources of stress. Take some L-Theanine in addition to the green tea.

(L-Theanine does the opposite of caffeine; but coffee is good for you overall). If you’re already too agitated, I guess it might help.
(HT)

Take Phosphatidyl Serine

If there is one supplement I’d recommend for its stress mitigating effects this would be it. The body doesn’t make much of it and we don’t get much from our diets, but its particularly concentrated in and is vital to the healthy functioning of nerve cell membranes. And get this: stress depletes it. PS is one of those 21st century hacks I’m always on the lookout for. It works on both mental and physical stress; improving mood and blunting cortisol after physical exercise.

Looks like the evidence for memory/cognition improvement is extremely weak, but the evidence for athletic performance (better recovery and reduced stress in competition) is good.

PS can be found in meat, but is most abundant in the brain and in innards such as liver and kidney. Only small amounts of PS can be found in dairy products or in vegetables, with the exception of white beans.

Food	PS Content in mg/100 g
Bovine brain	713
Atlantic mackerel	480
Chicken heart	414
Atlantic herring	360
Eel	335
Offal (average value)	305
Pig’s spleen	239
Pig’s kidney	218
Tuna	194
Chicken leg, with skin, without bone	134
Chicken liver	123
White beans	107
Soft-shell clam	87
Chicken breast, with skin	85
Mullet	76
Veal	72
Beef	69
Pork	57

fasting was also found to reduce other cardiac risk factors, such as triglycerides, weight, and blood sugar levels…

 

HGH works to protect lean muscle and metabolic balance, a response triggered and accelerated by fasting.During the 24-hour fasting periods, HGH increased an average of 1,300 percent in women, and nearly 2,000 percent in men.

(HGH is abused by some bodybuilders and is of questionable benefit in actually growing huge muscles)

 - Routine Periodic Fasting Is Good for Your Health, and Your Heart, Study Suggests

Potentially crackpot (no research cited) claim for improving low testosterone via diet:

• Restrict sugar
• Eat foods that inhibit aromatase (to limit oestrogen conversion)

(mushrooms and vitamin C inhibit aromatase - again, no study cited)

• Eradicate trans fats (via elimination of vegetable oils)
• Eat more fat - well less PUFA and more SFA

Fine. Butter is good for you. But EPA and DHA (Omega-3 and thus PUFA) are necessary in the diet.

• Eat foods that are rich in vitamins A+K (meat, butter, eggs, organs)
• Boost vitamin D

I started to get a little body acne after supplementing with 4000 IU D daily (especially once I started getting an hour of sun daily). I figured that was due to excess D (it’s fat soluble and so a dose that was fine for a few weeks may be too much once you’re saturated) but perhaps it was just giving me steroid-like side effects :) In any case, I cut back on the D supplementation (you can’t get too much D from sun, fortunately - the body scales back when it’s not needed).

Don’t worry yet about high-Choline diet causing high markers for heart disease.

(could be motivated cognition causing him to conclude “keep eating eggs and liver”, but there is a lot of evidence that insufficient Choline makes you dumber)

Men tend to think women find bulkier men attractive than what women generally find attractive (Frederick et al. 2005)

(evolvify - overuse of evo-psych story-time thinking warning). Yep. Marketing and a desire for high status; confusing physical power for it (not really the case in modern civilizations).

Humans are also good at assessing strength based on the face alone … subjects were just as good at judging strength from the faces of men of other cultures as from their own

Overall, body attractiveness was a better predictor of self-reported mating success than facial attractiveness. In line with our main hypothesis, we found a positive relationship between a composite measure of men’s physical fitness (PF) and men’s body attractiveness. This was obtained not only for aggregated attractiveness ratings but also for all 27 female raters individually. This finding is remarkable because individual attractiveness judgments reflect a strong idiosyncratic component, at least for faces. Attractiveness judgments were made fast and effortless. The strength of the attractiveness-fitness relation- ship obtained here suggests that signalling physical fitness may be one of the key functions of male attractiveness.” (Honekopp et al. 2006)

fitness, not bodybuilder bulk.

Multiple studies have confirmed that women are overwhelmingly more likely to cheat on their partner during the two or three days of ovulation. During this time, hormones alter a woman’s behavior to the point thatotherwise rational and emotional arguments against cheating are fundamentally altered. Emotions, culture, and society may be telling her that cheating is bad, but her body is telling her to mate with the best man she can get. Here’s the rub: The idea of what constitutes “the best man” also changes during that time.

(high-fitness, more “manly” men are sexier when a woman is fertile; she wants those good genes)

Conventional wisdom aside, it’s generally thought that people universally prefer lighter skin and (lesser known) yellower skin, which is a sign of high carotenoids, which are a sign for (cause of, probably) a healthier immune system. So it would make sense that people instinctively prefer yellower skin. Perhaps the fake orange tan is more attractive than a real tan, mockery of Jersey Shore notwithstanding. Anyway, it turns out that the yellow-skin preference is much stronger than the light-skin preference. Perhaps vegans are attractive after all, in spite of their low-protein diet and thus low-muscle body.

However, we have to trust that the photoshop color adjustment of face photos is faithful to actual tanning and high-carotenoid skin responses.

a higher skin content of carotenoids may reduce both the tendency to burn and the need and production of melanin

(anecdotal evidence) (HT)

Left, sun tan; center, neutral; right, carotene-rich

People consuming diets rich in carotenoids from natural foods, such as fruits and vegetables, are healthier and have lower mortality from a number of chronic illnesses.^[3] However, a recent meta-analysis of 68 reliable antioxidant supplementation experiments involving a total of 232,606 individuals concluded that consuming additional β-carotene from supplements is unlikely to be beneficial and may actually be harmful,^[4] although this conclusion may be due to the inclusion of studies involving smokers.^[5] With the notable exception of Vietnam Gacand crude palm oil, most carotenoid-rich fruits and vegetables are low in lipids. Since dietary lipids have been hypothesized to be an important factor for carotenoid bioavailability, a 2005 study investigated whether addition of avocado fruit or oil, as lipid sources, would enhance carotenoid absorption in humans. The study found that the addition of both avocado fruit and oil significantly enhanced the subjects’ absorption of all carotenoids tested (α-carotene, β-carotene, lycopene, and lutein).^[6]

(Wikipedia)

Carotenoids (tetraterpenoids)

Carotenes - orange pigments

α-Carotene – to vitamin A, in carrots, pumpkins, maize, tangerine, orange.

β-Carotene – to vitamin A, in dark, leafy greens and red, orange and yellow fruits and vegetables.

Lycopene – Vietnam Gac, tomatoes, grapefruit, watermelon, guava, apricots, carrots, autumn olive.

Phytofluene – star fruit, sweet potato, orange.

Phytoene – sweet potato, orange.

Xanthophylls - yellow pigments.

Canthaxanthin – paprika.

Cryptoxanthin – mango, tangerine, orange, papaya, peaches, avocado, pea, grapefruit, kiwi.

Zeaxanthin – wolfberry, spinach, kale, turnip greens, maize, eggs, red pepper, pumpkin, oranges.

Astaxanthin – microalge, yeast, krill, shrimp, salmon, lobsters, and some crabs

Lutein – spinach, turnip greens, romaine lettuce, eggs, red pepper, pumpkin, mango, papaya, oranges, kiwi, peaches, squash, legumes, brassicates, prunes, sweet potatoes, honeydew melon, rhubarb, plum, avocado, pear.

Rubixanthin – rose hips.

Basically, any colored fruit or vegetable (maybe clorophyll is so strong that you can’t really see the orange or yellow pigment - it just makes the result look “dark green”)

Carotenoids are fat-soluble so we must consume fats with carotenoid-rich foods to optimize carotenoid absorption.

I didn’t realize that fat-soluble meant you absorb it better when you have fatty acids from diet (in bloodstream? in digestive tract?). But I checked and it seems to be conventional wisdom. I thought fat-soluble only meant that you’d store it in your fat cells and thus release it when you burn fat for calories (that must be true).

A yet-unidentified component of coffee interacts with caffeine, a possible reason why daily coffee intake protects against Alzheimer’s disease, researchers at the 

University of South Florida have found.

One clue: they found that caffeinated coffee induces an increase in blood levels of a growth factor called GCSF (granulocyte colony stimulating factor) in mice. GCSF is greatly decreased in patients with Alzheimer’s disease and is demonstrated to improve memory in Alzheimer’s mice.

The researchers said this is not possible with other caffeine-containing drinks or decaffeinated coffee.

An increasing body of scientific literature indicates that moderate consumption of coffee also decreases the risk of Alzheimer’s, Parkinson’s disease, Type II diabetes, and stroke. Recent studies have reported that drinking coffee in moderation may also significantly reduce the risk of breast and prostate cancers.

The researchers suggest that moderate daily coffee intake (4 to 5 cups a day) starting at least by middle age (30s–50s) is optimal for providing protection against Alzheimer’s disease, although from their studies, starting even in older age appears protective.

Ref.: Gary Arendash, et al., Caffeine Synergizes with Another Coffee Component to Increase Plasma GCSF: Linkage to Cognitive Benefits in Alzheimer’s Mice, Journal of Alzheimer’s Disease, 25(2), June 28, 2011

HT

Presumably various types of tea have been tested and found wanting in boosting GCSF. Low GCSF is definitely diagnostic for Alzheimers, and elevating GCSF improves symptoms some.

This is causal. Usually you just see correlations, which leave open the possibility that only if you’re the type of person who was already likely to drink coffee, would you benefit - if you drank coffee only because you heard it was correlated with better health, then it would not work for you.

There are definite short-term changes in thinking from coffee (and probably caffeine in general) that are more tradeoffs than unambiguous improvements (supposedly creativity and long-term learning are impaired) - LessWrong discussion.

A meta-review

 

by A. Aeron-Thomas and S. Hess looked at the results of 10 studies. They found that total injury crashes fell by a significant amount in intersections that installed RLCs (estimates ranged from 13 to 29 percent). The reduction in total crashes was smaller for reasons I’m about to discuss, but it ranged from 7 to 26 percent. They concluded that RLCs reduce total casualties, though the reductions in total collisions are more modest.

Another study, this one from the Federal Highway Association, also found overall safety benefits. It concluded that right-angle crashes drop by about 25 percent when RLCs are installed. However, echoing a complaint frequently made by RLC detractors, it did find that rear-end collisions increased as drivers were more likely to slam on their brakes at the sight of a red light and get hit by the following car. Thus rear-end collisions tend to rise by about 15 percent.

However, right-angle crashes are far more dangerous and damaging than rear-enders, which explains why the study found that, on average, each RLC generated a net savings in crash costs of about $39,000 per year.

HT

Net savings after the cost of running the cameras. I wonder what the cost is, if any, in increased commute time.

I do think that rolling right-on-red should be allowed (not punished by RLC). The risk to pedestrians crossing at the time from inattentive drivers who feel free to roll-right-on-red is terrible, though.

In general, intersections would work better if:

1. there were pedestrian-recognition sensors (would likely have to be optical; whether active like radar, or passive like regular image recognition) that signal (especially for right-on-red turners) the presence of pedestrians. most of us have a habit of consciously checking for pedestrians at intersections, but not everyone does.

2. there were omnidirectional indicators of time-until-next-change. you already almost get this with the time counted on don’t-walk signals (once you know an intersection).

3. it were legal to run a red light after stopping if there are no other cars waiting (and obviously, without interfering with any moving cross traffic). many of us have done this late at night with no ill effects.

4. car-presence sensors were more universally employed, and worked more reliably for bicycles and motorocycles (just make them properly sensitive)

5. yellow light durations were indicated in some analog fashion (progress bar)

If you ever find yourself driving in Boston it has almost become customary for you to allow the first car in the turn lane to “bang a left” in front of you before you pull forward from the light.

Not sure about that one. If that were the custom, people going straight would have to get used to a slow start (as the quote suggests). I sometimes accelerate quickly when my light turns green (but only after actually checking for red light runners and left-bangers).

When asked to speculate on the biological mechanism, Krystal said that tumor cells, unlike normal cells, need significantly more glucose to grow and thrive. Restricting carbohydrate intake can significantly limit blood glucose and insulin, a hormone that has been shown in many independent studies to promote tumor growth in both humans and mice.

http://www.eurekalert.org/pub_releases/2011-06/aafc-lhd061411.php

High protein diets also tend to give better satiety per calorie, and help (up to some point of diminishing returns) funnel excess calories into muscle mass rather than fat.

(HT)

From Seth Roberts:

A new study in JAMA found higher salt consumption strongly associated with less death from heart disease. The association with total mortality (more salt, less death) was almost significant.

Add physical exercise to the list of possible confounds for the apparent truth that even heavy drinking (of alcohol) is healthier than abstinence (other likely candidates: a social life):

“Light, moderate, and heavy drinkers worked out 5.7, 10.1 and 19.9 minutes more per week, respectively. Also, drinking resulted in a 10.1 percent increase in the probability of vigorous physical activity.”
(http://www.livescience.com/7910-exercisers-drink-alcohol.html)

The study was published here.
(http://www.healthpromotionjournal.com/publications/journal/ib2009-09.htm)