Help Kronos' Chris Heward fight his cancer

Chris Heward past away on January 10, 2009. This post will remain here to remember Chris and his struggle against cancer.

John Schloendorn, who is a  postdoc at ASU’s Biodesign Institute and doing scientific research on the LysoSENS project for the Methuselah Foundation, asks you to support Chris Heward’s fight against cancer.

A new Facebook group to support Chris in his fight has been created here.

The white blood cell donor screening form is located here.

Dear all,

My friend Chris Heward was diagnosed with Stage IV terminal esophageal cancer. His chances of surviving a year are less than 1%, even with the best available care. For those of you who don’t know Chris, he is the president of the Kronos Science Laboratories, a Phoenix-based anti-aging hub

http://www.kronoslaboratory.com

Those of you who do know Chris will understand that he is not going down without a fight. Chris has very much the power of Kronos behind him, and we all hope that the experimental effort being launched there will not just benefit Chris, but many other sufferers of terminal cancers.

Plan A is based on the granulocyte therapy developed by Zheng Cui. Many of you know Zheng as well, and will remember that he made headlines throughout the anti-aging communities last year by achieving a complete cure for all types of cancer tested in the mouse.

A brief recap: Zheng by accident discovered that one of his mice was immune to any transplanted mouse or human cancers. This remarkable animal resisted a million times the dose of cancer cells that is 100% lethal to other mice. The trait turned out to be heritable in a single-gene mendelian fashion, but the responsible gene has so far resisted discovery. The cancer resistance was mediated by leukocytes, probably mostly of the granulocyte type. Granulocytes from the cancer-resistant mice chase cancer cells in a petri dish and destroy them. Granulocytes from other mice do not do that. Transplantation of granulocytes from cancer-resistant mice into other mice can transfer the cancer immunity, as well as cure existing cancers of all types tested (which were many types!). When Zheng looked in people, he found: Granulocytes form cancer patients never chase cancer cells. Granulocytes from healthy people sometimes chase cancer cells. Granulocytes from people in cancer-free families often chase cancer cells.

In September 2008, at the Methuselah Foundation sponsored “Aging 08” conference at UCLA, Zheng announced the launch of a clinical trial investigating the therapeutic effect of transplanting granulocytes from cancer-free donors (apt at chasing cancer cells in petri dishes) into cancer patients. A video of Zheng’s Aging 08 talk discussing all this in more detail is available here:
http://www.vimeo.com/1650186

Shortly after Aging 08, Zheng’s trial was put on hold by the FDA for certain bioethical concerns they had, and has been on hold since. Unfortunately, it is quite normal for this agency to charge ahead with the speed of a glacier. Chris does not have that kind of time. Our friends at Kronos are now scrambling to revive Zheng’s technology and apply it to Chris in the few months he has left. However, even for Kronos, this is not possible without your help. Here are a couple of ways:

*(1) Donate granulocytes*
The most critical resource for this project are granulocyte donors. The granulocyte donation process itself is harmless and simple for the donor. Granulocyte transplantation is in routine clinical use to treat a variety of infections. However, for Zheng’s therapy, many donors are needed to treat one patient, and the donors have to be selected for limited blood type and immune system compatibility. Thus, a fairly large number of individuals must be screened. If you get selected, the benefits will include adequate payment, possibly a free trip to Zheng’s facility at Wake Forest, Florida, and – in my opinion best of all – knowing whether your granulocytes possess the cancer-chasing ability. Oh yes, and who knows, maybe help discover the cure for cancer. Please complete the attached form to participate in the first round of screening. Send it to Wendy at Kronos: Wendy.Bezotte@kronoslaboratory.com Her email address and (shared!) fax number are also given on the form. I sent mine today.

*(2) Forward this message*
To reach a large enough number of donors, please forward this information to as many people as you can. Chris values his life a lot more than his privacy, and is explicitely asking us to launch this as a chain email. If you have a blog, blog away. If you’re a rockstar, announce it on stage. Don’t forget to attach the form. Or pour sacks of them into the audience.

*(3) Wish Chris well*
Chris has set up a Facebook page where he tells his story in a more personal way, and posts updates. Search “Chris Heward” and you will find him — he’s the smiling bald guy. If you would like to help in other ways, email Wendy directly, Wendy.Bezotte@kronoslaboratory.com

That’s all folks. Let’s see what we can do.

John Schloendorn

BioTime's quest to defeat aging

Unless you are a long-time cryonicist or a surgeon, you may not have heard of BioTime before. This company, recently profiled for its innovative stem cell research in Life Extension Magazine, is best known for producing the blood-volume expander Hextend, which was initially developed by Trans Time, an early cryonics company performing ultra-profound hypothermia research. Realizing the potential for Hextend’s conventional medical applications, BioTime was formed and, as they say, the rest is history.

These days, BioTime does its best to distance itself from its early history. As documented in this 2004 WIRED magazine article, BioTime prefers to downplay its (prior) relationship with Trans Time even though the association is well documented. Furthermore, their development of products like Hextend and its modification HetaCool, which can be used as a blood substitute to allow cooling to ultra-profound hypothermic temperatures for heart and brain surgery, as well as newly-developed HetaFreeze, a cryoprotectant solution used for long-term tissue and organ preservation at sub-zero temperatures, point to their cryonics past.

But things are changing at BioTime. Under the direction of CEO Dr. Michael West, and capitalizing on the highly successful sales of Hextend and related products, the company is now heading in a new direction: regenerative medicine. Dr. West, who received his Ph.D. from Baylor College of Medicine in 1989 concentrating on the biology of cellular aging, is pushing the envelope of aging research by developing new forms of stem cells that can be used to reverse cellular aging, perhaps eventually leading to the ability to reverse aging of the entire human body.

In “Regenerative Medicine Breakthroughs: Will BioTime Reset the Clock of Aging?” (November 2008), Life Extension Magazine documents Dr. West’s mission — to understand how to make somatic (i.e., body) cells immortal and then apply this technology to the treatment of aging and aging-related diseases. BioTime is now driven by the potential for stem cell therapy to repair and regenerate organs and tissues and, if possible, to radically extend human lives.

To understand the problem of cellular aging, we must first know what happens to cells as they age. One of the most important contributions in this field was first made by Alexy Olovnikov in the early 1970s, who proposed that the DNA sequence at the ends of each chromosome (called a telomere) shortened each time a cell replicated. Once the telomeres “ran out,” the cell stopped dividing. Olovnikov also theorized that germ (i.e., reproductive) cells, whose telomeres never shorten, do not age due to the production of an “immortalizing enyzme.”  Dr. West became so convinced of Olovnikov’s theory that he formed a company called Geron to investigate it further. As reported by Life Extension Magazine:

“Forty million dollars later,” West recalls, “the gamble paid off.” West’s group had in fact produced Olovnikov’s mysterious enzyme, now known as telemorase, because of its ability to continuously spin out the vital strands of telomere DNA that keep germ cells immortal.

However, getting telemorase into aging cells is easier said than done. Instead of attempting what basically amounted to gene therapy, Dr. West decided to take another route to cell immortalization: stem cell therapy. Because embryonic stem cell research has been so controversial, Dr. West and his team at BioTime are using a technique developed by researchers at Kyoto University to create stem cells from aged somatic cells. In this procedure, transcription factors are removed from egg cells and placed in somatic cells, which transform back into colonies of stem cells over a few weeks’ time, effectively reversing the aging clock in those cells. These cells are then called induced pluripotent stem cells (iPS). They function exactly like embryonic stem cells, but do not come from an embryo.

“And since numerous papers on iPS have now shown switching on the telemorase gene in these cells,” continues Dr. West, “I believe that within the next 12 months, the scientific community will have documented, for the first time ever, the reversal of aging of a human cell.”

Dr. West’s team at BioTime still has a long way to go, however. For starters, they are trying to figure out how those stem cells “decide”  what type of cell to become. With this information, the researchers can better direct stem cells in regenerative therapies to the correct tissue or organ needing repair. Reversal of aging of distinct cell populations could lead to reversal of aging of the entire human body.

Of course it should be noted that one of the many scientific feats cryonics depends upon to succeed is regenerative medicine: it would not be ethical or practical to revive an aged cryonics patient to live in a frail and diminished state. So it seems that BioTime may eventaully be reunited with its roots….

PLAC blood test for sudden cardiac arrest and stroke risk

Life Extension Foundation (LEF) unveiled a new blood test in an article in this month’s Life Extension Magazine (November 2008). Unlike cholesterol testing, which simply gives a measurement of high-density (HDL) and low-density (LDL) lipoprotein levels and provides little information about acute risk of stroke or heart attack, the PLAC® blood test “can accurately identify artherosclerotic plaque that is vulnerable to rupture,” essentially providing a direct assessment of sudden heart attack and stroke risk.

The PLAC® test, developed by diaDexus, Inc., provides this assessment by measuring levels of lipoprotein phospholipase A2 (Lp-PLA2), an enzyme that is directly involved in endothelial dysfunction leading to atherosclerosis (an inflammatory response of the blood vessel wall), plaque accumulation (build-up of lipid deposits inside blood vessels), and rupture (breaking loose of plaque which can then block a blood vessel, causing heart attack or stroke). The PLAC® test specifically measures Lp-PLA2 associated with oxidized LDL particles. In research studies, high levels of Lp-PLA2 have been determined to be highly specific for plaque inflammation: an elevated PLAC® test indicates an increased amount of inflamed atherosclerotic plaques and thus a higher risk of plaque rupture.

Because of the sensitivity and high specificity of the PLAC® test for such inflammation, the predictive value of the test for risk of cardiac arrest and/or stroke is higher than other markers for the prediction of acute events. Furthermore, the PLAC® test is inexpensive and convenient in comparison to CT and other imaging procedures since it involves only the collection of a blood sample.

In general, the PLAC® test is appropriate for those known to be at high risk for cardiovascular disease and stroke, and LEF recommends that it should be performed once a year in persons who are obese or are regular smokers, those with high blood pressure or cholesterol, type 2 diabetes, or a family history of stroke and coronary heart disease. The PLAC® test can be used to guide patient treatment options: from their article, the LEF panel “recommends that patients with high Lp-PLA2 levels be upgraded from moderate risk to high risk, or from high risk to very high risk. In these patients, a suitable goal is to lower LDL to 100 mg/dL in high-risk patients and to 70 mg/dL in very high-risk patients.”

The PLAC® test is currently the only blood test approved by the FDA to assess atherosclerotic risk for coronary heart disease and stroke. While this is useful for guiding patients in their use of known treatment options, it is not known whether lowering Lp-PLA2 itself will result in a reduction of this risk. A large study (IBIS-2 trial) is now underway to shed more light on this topic. In the meantime,  LEF claims that the PLAC® test is by far the most reliable, convenient, and inexpensive method for determining one’s risk of acute ischemic cardiovascular events and is undoubtedly a beneficial tool for helping patients to keep tabs on their risk level and to implement a more aggressive treatment strategy if indicated.

-=Get the PLAC® blood test=-

Antioxidant skepticism

At the blog Fight Aging!, Reason draws attention to the possibility that taking large amounts of antioxidant supplements may not necessarily be an improvement:

Our biology is complex – why would we expect that successfully modifying it with chemicals would be as simple as eating those chemicals? Ingesting antioxidants in the hope of benefit because they happen to do certain things in certain portions of your biochemistry is magical thinking given the evidence on the table to date.

And as the author points out, and contrary to popular perception, free radicals play positive roles in the human body as well. A similar point was made by critical care researcher and cryonics activist, Dr. Steve Harris on usenet in 2002:

Free radicals are the signals used by the body’s inflammatory system, which is necessary for infection-fighting, normal healing, and for fighting some (not all) kinds of cancer.  Free radicals (including deliberately produced ones like NO) aren’t just garbage to be expunged in every possible way you can think of, but rather instead are often important signals, not to be ignored. You can’t just willy-nilly shotgun them, and the system which uses them, out of existence for long, without expecting to pay a price. Nature didn’t give it all of that complicated radical-producing and radical-sensing machinery to you, for nothing.

Dr. Harris himself observed the price that may be paid when he participated in the Critical Care Research canine cerebral resuscitation experiments:

I’ve given large doses of vitamin E, melatonin, PBN, NOS inhibitors, COX inhibitors, basically the anti-radical anti-inflammation works, to dogs in resuscitation trials. This works great on the brain but occasionally I see a dog get pneumonia, and some of them die from it, with complete lung consolidation, in as little as 12-24 hours, despite heavy IV antibiotics. And in a very odd way: no fever, no left-shifted neutrophils, no increased heart rate, no shock (except at the hypoxic end). The last time I saw anything like that as a physician was treating leukemic patients with no neutrophils. These dogs have neutrophils, but they’re just not working.

Aggressive antioxidant treatment has a place in the treatment of stroke and cardiac arrest but to implement such an aggressive regime in the hope of fighting aging may be wishful thinking at best, and dangerous at worst. In general, many claims about the beneficial effects of dietary supplements should be approached with skepticism.

Any credible future treatment to slow or reverse aging will require interventions that specifically target the mechanisms of aging and/or remove their damaging effects without disturbing the general biochemistry of the human body. Whether such interventions will be possible without advanced nanomedical modification of human biology remains to be seen.

No disease in the brain of a 115-year old woman

In August 2008, Neurobiology of Aging published the interesting observations of den Dunnen, et al. of the post-mortem body of a 115 year old woman, which showed no evidence of atherosclerosis. Her brain was devoid of the amyloid plaques characteristic of Alzheimer’s disease and neural density was on par with healthy persons 60-80 year of age. Pre-mortem psychological testing of the woman at ages 112 and 115 found her cognitive abilities to be well above average, scoring better than the average healthy 60-75 year old. Indeed, the authors describe her repeatedly as “alert and attentive” and interpret their findings as follows:

“Our observations indicate that the limits of human cognitive function extend far beyond the range that is currently enjoyed by most individuals and that brain disease, even in supercentenarians, is not inevitable.”

This lack of pathophysiology and retention of mental abilities in old age is encouraging and should motivate us to take the best care of our bodies as possible, so that our latest years remain some of our best ones. However, it should be noted that while the woman’s Mini Mental State Examination (MMSE) score only dropped one point (from 27 to 26) from age 112 to 115, and her immediate recall ability and orientation did not deteriorate, she performed worse at age 115 at more complex tasks such as those testing working memory and mathematical calculation skills. In addition, though no amyloid deposits were found in her brain, the other hallmark of AD, neurofibrillary tangles, were observed in the medial temporal lobe, possibly indicating the very earliest stages of AD.

While brain disease at 100 may not be inevitable, and we will certainly enjoy our healthy lives as long as we have them, ultimately even the healthiest supercentenarians succumb to the progression of aging and its entourage of aging-related diseases. Cracking the mystery of aging will require multiple approaches, and studies of the oldest-lived among us provide clues as to which lines of inquiry are the best leads to follow.

Dietary supplements induce neurogenesis after stroke

A recent study in Rejuvenation Research reports that a combination of dietary supplements confer neuroprotection in stroke. Over a 2 week period rats received either a proprietary formulation of blueberry, green tea, Vitamin D3, and carnosine  called NT-020 or vehicle (i.e., the same solution minus the compounds of interest) before stroke was induced through middle cerebral artery occlusion (MCAo). Two weeks after the insult the rats were subjected to behavioral tests and histological examination. Rats treated with the dietary supplements scored better on behavioral tests, had less histological damage, and showed evidence of neurogenesis.

This study is interesting for a number of reasons. Foremost, it highlights the possibility that dietary choices can positively affect outcome after ischemic insults. These findings complement research that found that caloric restriction improves behavioral and histological outcome after stroke.  The findings also reinforce that some of the most effective neuroprotective agents to date are ordinary nutrients, vitamins, and hormones. In this study the investigators combine a number of these agents to greater effect. Although the authors do not present specific data on bioavailability in the brain for these compounds, they argue that a multi-agent approach relaxes the dosage requirements for individual agents.

The paper reviews assays that demonstrate improved neurogenesis in the rats that received NT-020 such as endogenous birth of new neurons, neuronal phenotype expression of newly formed cells, and alterations in neurogenic factors. Pharmacological modulation of neurogenesis after ischemia is a young research field and the results reported in this paper provide additional evidence for the (only recently accepted) phenomenon of adult neurogenesis. Unresolved questions at this point include how neurogenesis differs among species and whether post-ischemic neurogenesis can improve long term outcome in humans.

The  design of the current study does not allow a rigorous answer to the question of whether neurogenesis contributed to or accompanied improved outcome. The possibility that other mechanisms (such as  increased free radical scavenging) were primarily responsible for the observed improvements cannot be ruled out based on this study.

Link: Dietary Supplementation Exerts Neuroprotective Effects in Ischemic Stroke Model

Revitalize aging feet

My mother, being a decidedly well put-together woman, impressed upon me the importance of self-care from an early age. She was obsessed with skin maintenance and especially careful to instruct me in hand and foot care. I was given my first bottle of moisturizer at the age of fourteen (“I heard your skin starts losing its elasticity at that age”) and vividly recall sharing in an invigorating bi-weekly foot soak and pedicure. Later on, after developing severely fallen arches (aka “flat feet”) and enduring the pain associated with that condition, foot care became an especially important part of my self-care routine and I have since become somewhat of a foot care proselytizer.

As such, I was delighted to see an article entitled “Revitalize Aging Feet: The Importance of Proactive Foot Care” in the latest issue of Life Extension Magazine. This article, by Dr. Gary Goldfaden, begins with a spiel that I also frequently employ, alerting readers to the fact that the feet are the most overworked and undercared for part of the human body. For these reasons, our feet are particularly susceptible to injury, fatigue, infection, and skin aging –more so as we age and they lose their protective fat cushioning and have been exposed to a lifetime of ultraviolet radiation.

But, as with most things related to the body, an ounce of prevention is worth a pound of cure. Preventative foot care can not only make your feet look better, it can also lessen pain and muscle fatigue, which ultimately makes your entire body feel better.

As Dr. Goldfaden points out, many commercial foot creams consist primarily of water, which only serves to “plump up” the skin, thus smoothing out wrinkles, for as long as the water remains. Additionally, many of these products also contain oils that can actually increase free-radical oxidation and accelerate skin aging! Fortunately, there are some natural products that can significantly improve the look and condition of the feet.

Essential oils such as eucalyptus and menthol are a great place to start. Eucalyptis oil contains a compound called 1,8-cineole, which helps facilitate the production of skin lipids (ceramides), an important factor in retaining moisture in the skin. Eucalyptus oil also serves to protect feet from microorganisms that cause odor and infection, and acts as a natural analgesic for soothing achy joints and muscles. Menthol is also an effective pain reliever, and has the added benefit of providing a cooling sensation which is very refreshing for tired feet. Both eucalyptus oil and menthol also have beneficial effects on foot circulation, increasing blood flow to the feet and promoting the delivery of oxygen and nutrients to the deepest layers of the skin.

Also discussed is tea extract, which is rich in anti-oxidants which can protect feet from oxidative stress and inflammation. Other properties of antioxidant tea blends, such as their vitamin C activity, are also believed to contribute to improved skin tone and structure by strengthening connective tissues. Squalene, found in olive oil, is a natural emollient that hydrates and nourishes tissue while also providing anti-oxidant effects and inhibiting the proliferation of microorganisms. Coconut oil has an abundance of medium chain triglycerides that are “almost identical to the medium chain fatty acids found in human sebum” and is also a proven antibacterial, antiviral, and antifungal agent. Last, but not least, shea butter is touted for its abundance of vitamin E, a powerful antioxidant that is known for its ability to diminish wrinkles and smooth skin tone. I have personally found that buying vitamin E oil from a pharmacy is also very cost effective and works wonders to keep my feet looking and feeling soft and supple.

While the LEF article is timely and full of good advice, I was somewhat disappointed that it did not discuss other aspects of preventative and therapeutic foot care such as wearing appropriately supportive shoes, inserts and orthotics, visiting a specialist in case of foot disorders such as flat feet or neuromas, and the benefits of massage and reflexology. Expect to see a follow-up at this blog covering these topics in the near future.

Recent developments in the treatment of Alzheimer's

The full text of the Life Extension Foundation magazine article (August 2008) describing the use of Enbrel for the treatment of Alzheimer’s disease and announcing LEF’s new Enbrel trial, is now available. As previously discussed, Enbrel (entanercept) has been shown to provide immediate benefits in Alzheimer’s patients, improving memory performance and less frustration and agitation within minutes of treatment.

The more recent publication (pdf document) of additional data from the same patients in the previously reported six month Phase II trial adds further evidence to these results, specifically noting a rapid improvement in the verbal fluency of patients undergoing weekly perispinal Enbrel injections. Additionally, case studies of two more patients are given in the text of the report, and a stronger case for carrying out larger scale studies (including Phase III clinical trials) is made.

A blog post at Al Fin reports on other promising Alzheimer’s treatments such as the drug Rember, which “appears to target ‘Tau tangles’ in the portion of the brain most active in memory formation.”

TNF-alpha modulation in Alzheimer's patients

More than a decade of basic research and clinical evidence now implicates inflammatory processes in the pathogenesis of Alzheimer’s disease (AD). TNF-alpha is a pro-inflammatory cytokine, also known as the “master regulator” of the immune response, and is the key initiator of immune-related inflammation in the brain. Much evidence has linked excess TNF-alpha to the development of AD, including the demonstration of 25-fold elevated levels of TNF-alpha in the cerebrospinal fluid of AD patients and the finding that beta-amyloid (the main constituent of the amyloid plaques found in the brains of AD patients) stimulates the secretion of TNF-alpha, which in turn induces beta-amyloid production in a vicious positive-feedback loop. This beta-amyloid-induced neuroimflammation has been shown to result in neurotoxicity and to upregulate other inflammatory mediators in the brain, including interleukin (IL)-1 beta, IL-6, and nitric oxide.

To examine the effect of downregulating this inflammatory process, a group of researchers performed a 6 month pilot study in 2006 to determine the effect of modulating TNF-alpha in AD patients using the specific anti-inflammatory agent entanercept (Enbrel). Enbrel selectively inhibits the biologic activity of TNF-alpha by binding to TNF-alpha and preventing its interaction with cell-surface TNF receptors.  Entanercept is already FDA approved for the treatment of such diseases as rheumatoid arthritis, psoriasis, and psoriatic arthritis.

Fifteen patients with mild to severe AD were evaluated before treatment began and once a month thereafter for six months using three standard measures of cognition: the AD Assessment Scale-Cognitive subscale (ADAS-Cog), the Severe Impairment Battery (SIB), and the Mini-Mental State Examination (MMSE). Treatment consisted of a total dose of 25 to 50 mg of Enbrel in sterile water per week via interspinous injection. This injection between two cervical vertebrae is hypothesized to improve flow of the drug to the central nervous system (CNS). All patients in this pilot study improved significantly on all assessments of cognitive ability, which is particularly amazing given the cognitive decline that would normally be expected of an AD patient over the course of six months.

As mentioned, this pilot study was approved to evaluate patients only at monthly intervals. However, during this six-month study and over the course of their clinical experience since the pilot study, the researchers noted “an unexpected and largely unprecedented clinical phenomenon… a noticeable clinical improvement within minutes of perispinal entanercept administration.” To validate these observations, the researchers performed a case study in 2008 in which a patient with severe AD was evaluated prior to, ten minutes after, two hours after, and one week after Enbrel administration.

Prior to treatment the patient had been unable to recall his birthday, his father’s occupation, or the names of any of the physicians treating him. He was not oriented to the calendar date, day of the week, year, place, city, or state. Ten minutes after receiving an injection of Enbrel, the patient correctly identified the state as California and his demeanor was observed to be calmer and more attentive. His responses to questions were less effortful, as well.

At the 2-hour post-evaluation, the patient was able to recall the name of his evaluator and was able to identify the month, day of the week, place, and name the state of California. He was slightly off on the calendar date and year, but “appeared more aware of his deficient performance.” The patient’s scores on all mental tests also improved dramatically. These improvements were maintained over the course of a week, whereupon he was evaluated again before receiving his next Enbrel dose. The patient continued to receive a weekly dose of Enbrel for a total of 5 weeks and was re-evaluated at 7 weeks (fourteen days after his last dose). His improvement in all areas of cognitive performance was marked and significant.

An important consideration when treating a patient with Enbrel, however, is that it is immunosupressive and as such leaves the patient at high risk of morbidity if they acquire an infection. This is especially important in late-stage Alzheimer’s patients, who are generally elderly, frequently visit hospitals/treatment centers, and live in community environments, making them particularly susceptible to community-acquired infection.

Following up on the publication of these unprecedented findings, the Life Extension Foundation recently published a review of both Enbrel pilot studies and the initial results of their own pilot study involving a 91-year-old female AD patient with severe cognitive deficits, who has also shown marked improvement in cognitive ability. The Life Extension Foundation is now eager to “launch an expanded study with the objective of measuring the long-term effects of weekly Enbrel injections plus nutrients that help suppress the production of excess TNF-alpha.” These trials are aimed at treating early-stage AD patients, and weekly Enbrel injections will be given in the Fort Lauderdale area.

To inquire about enrolling in this new study, contact the Life Extension Foundation.

Gary Taubes and bias in nutrition science

In a recent blog post, Overcoming Bias reports that Gary Taubes, who has written much to further the idea that refined carbohydrates are a stronger contributing factor to overweight and “diseases of civilization” than dietary fat and cholesterol, has compiled his thoughts on the subject in a major 600-page work called Good Calories, Bad Calories.

Why is Taubes so interested in bias?  For several decades, it has been the conventional wisdom that dietary fat (and especially saturated fat) contributes to obesity, heart disease, and cancer.  Judging from Taubes’ exhaustive research — indeed, I’d be surprised if any other book examined bias within a particular scientific field in such detail — the conventional wisdom was based on unreliable and slender evidence that, once established and institutionalized in government funding, set a pattern of confirmation bias by which further research was judged (or ignored).

Related: The Entitled to an Opinion blog on bad cholesterol and political correctness.