Forget Universal Health Care: Eat Your Ice Cream!

Ice cream researchers are converting the cold treat into a Trojan Horse for long life and vitality. They are learning to supplement the frozen delight with ingredients known to bolster the health of the cardiovascular, digestive, endocrine, and immune systems. And they are just getting started . . . .

Adding nutrients such as pro-biotics, which are already found in some dairy products, and fiber to ice cream can improve digestive health. Many diseases are caused by inflammation that starts in the intestines, Gruen said. Improving digestive health with functional foods might reduce that inflammation. Although functional foods have health benefits, there are many challenges to adding nutrients to ice cream.

"Our major challenges are texture, flavor and psychological acceptance," Gruen said. "The nutrients we add often have bitter tastes and affect the texture of ice cream that we have to mask. Flavors like chocolate are easier to work with because the flavor is so strong that it can overcome other flavors from the nutrients. Another challenge is determining whether people would be upset that we're 'tampering' with a comfort food. We need to know if they would be more willing to pay for ice cream with added nutritional benefits."

Gruen and his research team are looking at using the açai berry and remnants from grapes in wine-making to add nutrients to ice cream. They hope to have a prototype ready for tasting in the next six months. _SD

Al Fin nutritionists are unanimous in their support for this approach to good health. Whereas the health care bills before the US Congress threaten to destroy everything that is innovative and generative in the US biomedical system, health-promoting ice cream is merely food.

It is understandable why persons prone to premature senility and aging -- such as Speaker of the House Nancy Pelosi -- might be obsessed with matters of health, to the point of losing all sense of reason and proportion. But that is no reason to destroy the most innovative biomedical system in the world. Don't be such a jerk, Nancy! ;-)

But seriously, folks, the concept of using ordinary foods and beverages as vectors for evolutionary and revolutionary health improvements, is an idea long overdue. Mainstream food scientists think very small. Al Fin nutritionists think very big. Stay tuned.

Make Every Meal Fit for Royalty

There is a reason that fortunes were made and wars were fought throughout history over spice routes and salt deposits. We in modern countries have an abundance of spices and seasonings to suit our every whim. But are we taking best advantage of them?

“Because herbs and spices have a very low calorie content and are relatively inexpensive, they’re a great way to get a lot of antioxidant and anti-inflammatory power into your diet,” said study co-author James Hargrove, associate professor of foods and nutrition in the UGA College of Family and Consumer Sciences....

...The researchers found a strong and direct correlation between the phenol content of common herbs and spices and their ability to inhibit the formation of AGE compounds. Spices such as cloves and cinnamon had phenol levels that were 30 percent and 18 percent of dry weight, respectively, while herbs such as oregano and sage were eight and six percent phenol by dry weight, respectively. For comparison, blueberries – which are widely touted for their antioxidant capabilities – contain roughly five percent phenol by dry weight.

Study co-author Diane Hartle, associate professor in the UGA College of Pharmacy, said various phenols are absorbed differently by the body and have different mechanisms of action, so it’s likely that a variety of spices will provide maximum benefit.

“If you set up a good herb and spice cabinet and season your food liberally, you could double or even triple the medicinal value of your meal without increasing the caloric content,” she said.

She added that controlling blood sugar and the formation of AGE compounds can also decrease the risk of cardiovascular damage associated with diabetes and aging. She explained that high blood sugar accelerates heart disease partly because AGE compounds form in the blood and in the walls of blood vessels. The AGE compounds aggravate atherosclerosis, which produces cholesterol plaques. _PO

While you are adding healthy spices to your foods, you can also gain significant benefit by substituting potassium salts for sodium salt in routine food seasoning. The taste is quite similar to table salt, and persons of all ages and states of health (except kidney failure with high serum potassium) can safely take extra potassium.

Throughout most of human history, only a few lucky persons were able to enjoy most of the spices, beverages, and foods that are available to even the poorest person in the modern world. We are living in an epicurean age. Are we to blame if eating and drinking well can also be good for us?

Food, History, and Perspective

Image Source

Human lifespan is bumping into diseases of the brain such as Alzheimer's Dementia. Modern medicine is temporarily stymied as to how to deal with such problems of degeneration over time. You may consider it ironic that ancient herbs and spices may hold a key to dealing with this dilemma brought about by longer life.

The history of foods, spices, seasonings, and beverages makes a fascinating side-bar to the history of human settlements, trade, and conquest.

The quest for spice, was a huge motivation behind the competition of the various European peoples to lay claim to trade routes to the far east. It was this competition for favourable trade routes that led to the discovery of the Americas by 15th century Europeans, and the colonisation of the Americas, Africa, and significant parts of Asia and Oceania.

Even the humble seasoningsalt, played a very significant role in the trade and conquest of early people. At one time, salt was used as payment for services rendered. Hence the saying, "he is not worth his salt." The table below gives a rough overview of the history of human herbs, spices, and vegetables.

Mediterranean (Used B.C.)	Mushroom, beet, radish, turnip, carrot, parsnip, asparagus, leek, onion, cabbage,lettuce, artichoke, cucumber, broad bean, pea, olive, apple,pear, cherry, grape, fig, date, strawberry, basil, marjoram, oregano, mint, rosemary, sage, savory, thyme, anise, caraway, coriander, cumin, dill, parsley, fennel, bay, caper, fenugreek, garlic, mustard, poppy, sesame, saffron.
(Later)	Spinach, celery, rhubarb, cauliflower, broccoli, Brussels sprouts.
Asia: (Used BC)	Citron, apricot, peach, cardamom, ginger, cinnamon, turmeric, black pepper.
(Later)	Yam, water chestnut, bamboo, eggplant, lemon, lime, orange, melon, clove, nutmeg, mace, tarragon.
New World: (Used BC)	Potato, pumpkin, squash, tomato, kidney bean, lima bean, sweet pepper, avocado, pineapple, allspice, red pepper, chilli pepper, vanilla

_Source

When future humans look back on the fall of western civilisation, and its conquest by more primitive humans, they will likely wonder whether there was something in the drinking water that made us weak, or perhaps something in our diets?

Of course, next level humans will understand most of the multi-factorial reasons for the fall of enlightened, multiculturalised postmodern western society. But next level humans will probably be spending their time pushing the limits outward, lightyears beyond the pedantic and pedestrian scholars of future Earth--who try to understand the rise and fall of great empires of the past.

We should not forget to take what is important along with us, including the spices, foods, passions, and beverages that make an ambitious and accomplished life enjoyable.

You Could Have Had a V8!

Beetroot juice is one of the main components of V8 Juice, a popular vegetable drink in the US. The blood pressure lowering effect of beetroot juice has been explained by recent research:

Fourteen healthy volunteers were recruited for the study and asked to drink either 500 millilitres of beetroot juice or the same quantity of water within 30 minutes.

Their blood pressure was measured every 15 minutes from one hour before taking the drink to three hours afterwards....Thereafter readings were taken every hour for six hours. A final test was conducted 24 hours after the drink was consumed.

Volunteers who drank the juice started to show reductions in blood pressure after just one hour....After two and a half hours, their systolic rate - the pressure with each heartbeat - was around 10 millimetres of mercury (mm Hg) lower than that of participants who had drunk water.

For the diastolic reading - the "resting" pressure between heartbeats - a reduction of 8 mm Hg was seen in the juice drinkers after three hours....At 24 hours, systolic BP was still more than 4 mm Hg lower for volunteers given the beetroot, while there were no differences for diastolic BP.

The study's leader, Prof Amrita Ahluwalia, from the William Harvey Research Institute at St Bartholomew's Hospital, London, said: "Drinking beetroot juice, or consuming other nitrate-rich vegetables, might be a simple way to maintain a healthy cardiovascular system."___Telegraph

A person's saliva converts nitrates in the juice to nitrites, which when converted to nitric oxide causes vasodilation and reduction of blood pressure.

Nitrates are common pharmaceuticals used to treat various medical conditions where vasoconstriction is harmful. A stiff shot or two of beetroot juice--or low sodium V8--should help millions of hypertensives.

The Poor Man's TNF Blocker: Curcumin

Enbrel (Etanercept), an anti-arthritis drug, has recently been shown to improve cognition in Alzheimer's Disease patients, via Tumour Necrosis Factor (TNF) blocking. Even if Etanercept was approved for treating AD, a yearly dose of Enbrel would cost an Alzheimer's patient US $30,000 per year.

Curcumin (turmeric), a root spice used in Indian cooking, also blocks TNF. In addition, curcumin crosses the blood-brain-barrier readily. Prevalence of AD in Indian seniors is less than half the prevalence of AD in North Americans. Combining those facts suggests that Indians may be protected from Alzheimer's Disease by the contents of their diet, possibly via at least one of the same pathways that the drug Enbrel protects against AD.

In some studies in AD model mice, Beta Amyloid levels in mice given curcumin were reduced by 40% compared to levels in mice not given curcumin. Above a certain dose level of curcumin, the amyloid reduction affect of curcumin was diminished, however.

North American researchers have studied curcumin for protective effects in cancer and sepsis, and more recently have begun looking at curcumin for AD prevention. The common pathway for those diseases that is blocked by curcumin is our old friend, the NFkappaB pathway, triggered by TNF, among other things.

With the knowledge that AD is worsened by multiple TNF effects on glial cells in the brain, the importance of locating effective TNF inhibitors grows more urgent.

This article presents several other pharmacological effects of curcumin.

More information about the awakening of western medicine to Curcumin.

Nice article on curcumin by John Smart

Waiting to Make SENS of Aging, Life Extension, Longevity?

Many of you are familiar with Aubrey de Grey and his SENS approach to life extension and longevity. For the intermediate term, de Grey's approach offers a lot of promise in the fight against aging.

In the short term, we need something more immediate. Ray Kurzweil has written a book on aging, discussing the several dozen supplements he takes daily. Most people do not need that much, but some might need more. A recent Barron's article took a stab at the subject, and the last Technology Review featured an interesting article about research into the anti-aging gene sirt.

This brief posting will deal with the basics of life extension now, rather than longevity in the next fifty years. Several postings in Al Fin have dealt with this topic, and there is no need to repeat them. This is just the basics. People below the age of 40 should ignore the hormone section. Each person should selectively choose agents based upon his own circumstances. Inform yourself in basic biology. Consult professionals before taking prescription medicines or extremely high doses of any agent. Middle aged males with or without family history of prostate cancer: take androgens, DHEA, etc. at your own risk, or after consulting a professional.

1. Hormones: DHEA, Pregnenolone, HGH, androgens, estrogens, thymosin, melatonin, and thyroid.
2. Antioxidants: Vitamins A,C,E, Lipoic Acid, Selenium, NAC, CoQ10, polyphenols, other phyto-antioxidants.
3. Antiglycation agents: Aminoguanidine, Carnosine, pyridoxamine, benfotiamine, ALT 711.
4. Brain Boosters: Ginkgo, PS, bacopa, DMAE, neurotransmitter precursors, hydergine, vinpocetine, Huperzine, etc.
5. Calorie restriction mimetics such as resveratrol, quercetin, etc.
6. General: TMG, Curcumin, carnitine, B complex, etc.
5. Immune Boosters: Wide variety of herbals and complex carbohydrate derivatives of plants and microorganisms, plus a lot of laughter.
6. Physical exercise and prudent eating, plus elimination of clearly bad habits and institution of good lifestyle habits.
7. Mental and emotional training. Practise sentic cycles and other forms of meditation. Read books on mind and memory training, and practise exercises.

If you are too old to wait for SENS, but rebel against the need to practise self-discipline, simply get old as you are doing. Otherwise, consult the longevity links posted on the side-bar of the Al Fin main page. Learn what you can, and start practising what you can. The important thing is to take a systematic approach. If you take supplements, but smoke like a stack, drink like a fish, exercise less than a minute a week, and sleep only two or three hours a night, you may not be taking a balanced approach to the problem.

In a later post, I will go into more detail on some of the particular agents and approaches outlined above. In the meantime, feel free to utilise the source materials that are provided under "longevity" and "singularity".

Predicting Life Extension and Human Longevity

Over at the Speculist Blog, Stephen Gordon talks about the joys and perils of predicting trends in human longevity and life extension. Stephen once predicted--boldly, he felt--that 2014 would be the date for life extension to take off. Now Stephen is in the uncomfortable position of being upstaged by a biologist from Stanford, Shripad Tuljapurkar.

In this article, Dr. Tuljapurkar makes many interesting predictions concerning the effects on the world of increasing average lifespan past the 100 year mark. Overpopulation, increased inequality, a trend toward more serial monogamy, and the raising of the retirement age are some of his predictions. Dr. T. sets the date 2010 as the beginning of the rising lifespan.

The Speculist feels that a lot of unanticipated things will happen between now and 2010, and certainly between now and 2030. The Speculist represents a fairly optimistic blog-vision of the future. But read both the above article, and the reaction by the Speculist.

Personally, I feel that the acceleration has already begun. Not only are new drugs such as statins, ACEIs, ARBs, modafinil, donezepil, memantine, and many others changing many of the underlying processes of degeneration in the body and mind, but the process of new drug discovery is exploding rapidly. In addition, many people have gone on their own into personal life extension experimentation, taking pharmaceuticals and non-pharmaceuticals alike. Vitamin stores are happy to sell resveratrol, quercetin, carnosine, lipoic acid, Curcumin, DHEA, and other promising non-pharmaceuticals to an ever more sophisticated buying public.

Besides all that, a new generation of scientists has grown up with the idea that life extension is not wrong or unnatural, but is completely natural, ethical, and a worthy goal to pursue. These scientists are finding that the people who control the purse-strings are growing more agreeable as well. The tsunami has been spawned by the underlying groundswell, and will not be stopped. ETA: any time now.

Resveratrol, Quercitin, Calorie Restriction, Longevity

Scientific American's new issue contains an article about "longevity genes" and the search to unlock them. Many articles have been written about the Sir and Sirt genes known to influence longevity in yeast and lower animals. The recent SciAm article brings us fairly up to date on the research of the authors and their associates (David Sinclair and Lenny Guarente).

Calorie restriction (CR) was cited as one of the few maneuvers known to increase lifespan of laboratory animals. Not surprisingly, CR works through the Sirt genes. What was surprising was that resveratrol, found in red grapes and wine, also affects the Sirt genes in much the same way as CR.

First of all, the researchers had to dispense with an old theory that turned out to be false:
The phenomenon (life extension through CR) was long attributed to a simple slowing down of metabolism--cells' production of energy from fuel molecules--and therefore reduction of its toxic by-products in response to less food.

But this view now appears to be incorrect. Calorie restriction does not slow metabolism in mammals, and in yeast and worms, metabolism is both sped up and altered by the diet. We believe, therefore, that calorie restriction is a biological stressor like natural food scarcity that induces a defensive response to boost the organism's chances of survival. In mammals, its effects include changes in cellular defenses, repair, energy production and activation of programmed cell death known as apoptosis.

....Yet if humans are ever to reap the health benefits of calorie restriction, radical dieting is not a reasonable option. Drugs that can modulate the activity of Sir2 and its siblings (collectively referred to as Sirtuins) in a similar manner will be needed. Just such a Sirtuin-activating compound, or STAC, called resveratrol has proven particularly interesting. Resveratrol is a small molecule present in red wine and manufactured by a variety of plants when they are stressed. At least 18 other compounds produced by plants in response to stress have also been found to modulate Sirtuins, suggest?-ing that the plants may use such mole?-cules to control their own Sir2 enzymes.

....Feeding resveratrol to yeast, worms or flies or placing them on a calorie-restricted diet extends their life spans about 30 percent, but only if they possess the SIR2 gene. Moreover, a fly that overproduces Sir2 has an increased life span that cannot be further extended by resveratrol or calorie restriction. The simplest interpretation is that calorie restriction and resveratrol each prolong the lives of fruit flies by activating Sir2.

Resveratrol-fed flies not only live longer, despite eating as much as they want, but they do not suffer from the reduced fertility often caused by calorie restriction. This is welcome news for those of us hoping to treat human diseases with molecules that target Sir2 enzymes. But first we want a better understanding of the role of Sir2 in mammals.

....Increased Sirt1 (the mammalian version of Sir2) in mice and rats, for example, allows some of the animals' cells to survive in the face of stress that would normally trigger their programmed suicide. Sirt1 does this by regulating the activity of several other key cellular proteins, such as p53, FoxO and Ku70, that are involved either in setting a threshold for apoptosis or in prompting cell repair. Sirt1 thus enhances cellular repair mechanisms while buying time for them to work.

....Both our labs are running carefully controlled mouse experiments that should soon tell us whether the SIRT1 gene controls health and life span in a mammal. We will not know definitively how Sirtuin genes affect human longevity for decades. Those who are hoping to pop a pill and live to 130 may have therefore been born a bit too early. Nevertheless, those of us already alive could live to see medications that modulate the activity of Sirtuin enzymes employed to treat specific conditions such as Alzheimer's, cancer, diabetes and heart disease. In fact, several such drugs have begun clinical trials for treatment of diabetes, herpes and neurodegenerative diseases.

The authors were careful not to hype resveratrol, since the research is still ongoing. Other people working with CR are a bit more enthusiastic about resveratrol. Both resveratrol and quercetin have been known for a number of years now to influence Sirt genes. Vitamin and supplement makers are growing quite sophisticated in keeping up with research, and waste no time making natural phytochemicals available to the public, where legal.

It is unlikely that these phytochemicals represent a hazard to the public. Certainly I have been imbibing resveratrol in liquid form for several years now, with no untoward effects noted. Nevertheless, it is hazardous to the purse to buy every supplement that some vitamin salesman promotes. Follow the research and make up your own mind.

I recommend reading the Scientific American article in its entirety.

Alzheimer's Disease Puzzle: New Key to Prevention

For over a decade, scientists have known that apolipoprotein E4 (apoE4) is associated with susceptibility to Alzheimer's disease. Slowly, neuroscientists are accumulating more details about the actual mechanism by which apoE4 leads to neurological damage in Alzheimer's. In this ScienceDaily news release, Georgetown Neuroscientists, Rebeck and Hoe, present more details about this connection:

the research team specifically found that receptors on the outside of brain nerve cells (neurons) that bind on to APOE and glutamate are connected on the surface of neurons, separated from each other by only a small protein.

While the scientists don't know why these receptors are linked together, they say inefficient or higher-than-average levels of APOE in the brain could possibly be clogging these binding sites, preventing glutamate from activating the processes necessary to form memories.

"We have found out that two receptors previously thought to have nothing to do with each other do, in fact, interact, leading us to conclude that APOE affects the NMDA glutamate channel that is important in memory," says the study's senior author, G. William Rebeck, PhD, associate professor of neuroscience in Georgetown's Biomedical Graduate Research Organization.

...In work leading up to this study, Rebeck and the research team found that adding APOE to neurons in laboratory culture blocked NMDA receptors. In this study, they confirmed through a series of experiments that the receptors for APOE and NMDA interacted, and that the protein that linked the two was PSD95, often found in neural synaptic junctions. Together, they form a multiprotein complex that could presumably be activated by either APOE, NMDA or glutamate.

Rebeck suspects that the APOE4 variant — the one linked to Alzheimer’s disease — is less efficient at removing lipid debris in the brain than is APOE2 or APOE3, and because of this, brain cells secrete more of the faulty protein to do the job. If too much APOE ends up binding to the APOE/NMDA receptor, one of two things could possibly happen, Rebeck says. In one scenario, the receptor becomes over-stimulated due to the accumulating presence of APOE, which could trigger a process called excitotoxicity that results in death of the neruons. Or, in the presence of damage and secreted APOE, the receptor “turns down” its activity — thus, hampering memory formation — until the brain is repaired. “Having damage around tells the brain not to think too much for awhile,” Rebeck says. But if APOE4 cannot clear up accumulating damage, the ability to make new memories, and use old ones, may be increasingly lost.

Hat tip to Medicineworld.
Original newsrelease source

Other researchers are on this fertile trail. Chang, Ma, et al from UC San Francisco published this intriguing article examining the molecular mechanisms of neurotoxicity and mitochondrial dysfunction. The researchers looked at variants of apoE4, to determine the precise portion of the peptide chain that was responsible for the toxicity.

ApoE4(241-272) did not cause mitochondrial dysfunction or neurotoxicity, suggesting that the lipid-binding region alone is insufficient for neurotoxicity. Truncation of N-terminal sequences (amino acids 1-170) containing the receptor-binding region (amino acids 135-150) and triple mutations within that region (R142A, K146A, and R147A) abolished the mitochondrial interaction and neurotoxicity of apoE4(1-272). Further analysis showed that the receptor-binding region is required for escape from the secretory pathway and that the lipid-binding region mediates mitochondrial interaction. Thus, the lipid- and receptor-binding regions in apoE4 fragments act together to cause mitochondrial dysfunction and neurotoxicity, which may be important in Alzheimer's disease pathogenesis.

The full text article is available here.

Ben Best has provided a useful description of the possible mechanisms of Alzheimer's Disease. In this section he discusses the apoE4 connection. A woman with one APOE4 allele has 4 times the AD risk of a woman with no APOE4 allele. A person with two APOE4 alleles has as much as 16 times the AD risk [INTERNATIONAL JOURNAL OF CLINICAL PRACTICE 56(3):197-203 (2002)].

In this article, I discussed a novel treatment for Alzheimer's, which is effective for both moderate and severe Alzheimer's Disease. Since the drug Memantine blocks NMDA receptors, and is a more effective treatment for AD than the earlier cholinesterase inhibiting drugs, it is clear that a more profound understanding of the actual mechanisms for AD will lead to even better treatments, even effective prevention methods.

Please understand that prevention of Alzheimer's will have a much more profound effect on society as a whole, than an effective treatment. By the time the disease is diagnosed, much damage may already have occurred.

Now that we better understand part of the genetic susceptibility for AD, more people will opt for an early genetic diagnosis. But what good is knowing that you are susceptible to early or late onset Alzheimer's if there is nothing you can do about it? Of course, Ben Best and others talk about preventing Alzheimer's with nutrients and vitamins. Curcumin is considered a likely preventative, given the very low incidence of Alzheimer's in India, where curried foods are commonly eaten daily.

The latest research by Rebeck et al, and Chang et al, are intriguing to me for another reason. They suggest that many of the symptoms of Alzheimer's patients may very well be reversible--not yet permanent. In other words, many of the NMDA receptors necessary for learning may simply be overwhelmed by excess debris, but not yet destroyed. That would partially explain why many AD patients are better on some days than others. Take away the damaging waste products, and the brain "sobers up" temporarily.

Would I have myself tested genetically? Why not? Research is advancing quickly. Until efficient pharmaceuticals for prevention of AD are approved, there is always Curcumin.