[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.

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

(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 (<100g/day) may conversely improve glycaemic control.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.

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).

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.

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)

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.

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]

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

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.