Monthly Archives: February 2015

On cancer cells: “Most strikingly, our discovery that glucose withdrawal causes both cell death…


In cancer cells, glucose starvation activates a metabolic and signaling feedback loop leading to cell death. Glucose starvation induces generation of reactive oxygen species generation (ROS), thereby inhibiting phosphatases and activating tyrosine kinases, which in turn generate additional ROS. This glucose starvation-induced positive feedback loop amplifies ROS levels until cells undergo ROS-mediated cell death.

http://www.sciencedaily.com/releases/2012/06/120626131854.htm

Read the entire article from 2012!

Keeping blood glucose low with ketogenic diet may really kill cancer cells. There is research out there. Keep watching for it!

Resistance training (barbells) keeps aging brains nimble


http://www.stuff.co.nz/life-style/well-good/teach-me/66273400/weights-keep-brain-nimble-research-suggests

 

Weights keep brain nimble, research suggests
MATT STEWART
Last updated 05:00, February 17 2015

Pumping iron could be a powerful weapon in the fight against dementia, new research suggests.

The University of Sydney study shows resistance weight training could be crucial in keeping the ageing brain nimble, as working out with weights was found to boost the mental agility of older people with mild cognitive impairment – a common precursor of dementia that is not treatable with drugs.

Geriatrician Maria Fiatarone Singh, the study’s chief investigator, said weight training stimulated hormones that promoted muscle growth. “It’s possible these hormones are also having similar benefits for brain function,” Singh said.

One hundred participants did six months of weight training and showed a significant lift in overall cognitive function especially in planning, organising, strategising and visual memory.

The gains were still there a year after the training finished. “The next step is to see how long this lasts and who benefits most from such exercise,” Singh said.

Scientists will follow the group for up to five years to see if they can put off or even stop the onset of dementia. Predictions suggest 135 million people worldwide will suffer dementia-related brain diseases by 2050.

“But if a simple cost-effective exercise intervention can show this much promise, I think further research could dramatically reduce that number,” Singh said.

The study, published in the Journal of the American Medical Directors Association, compared the effects of weight training, computer-based brain training, and a combination of the two for people over 60 suffering the memory and processing losses linked to mild cognitive impairment.

University of Otago cognitive psychologist Liana Machado said the Australian findings complemented her research into healthy young adults. Even though the studies were different – one focused on weight training, the other on aerobic exercise – Machado said together they pointed to both weight training and aerobic exercise being good for the brain.

“The cognitive benefits gained from regularly engaging in exercise may stem from improvements in brain blood-flow regulation and oxygen availability in the brain,” Machado said.

 

Long-term effects of a ketogenic diet in obese patients


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2716748/

 

The present study shows the beneficial effects of a long-term ketogenic diet. It significantly reduced the body weight and body mass index of the patients. Furthermore, it decreased the level of triglycerides, LDL cholesterol and blood glucose, and increased the level of HDL cholesterol. Administering a ketogenic diet for a relatively longer period of time did not produce any significant side effects in the patients. Therefore, the present study confirms that it is safe to use a ketogenic diet for a longer period of time than previously demonstrated.

 

This is important news.

The ketogenic diet is not harmful and promotes the health of those who live a ketogenic life style. 

Hubby and I have been on this diet for almost a year and four months. We have lost 70 pounds between us and improved our lab tests, energy levels, sleep and have lost symptoms of some of our chronic disease such as psoriasis, arthritis.

We’re looking forward to a little more weight loss and health improvements as we age!!

It’s been great!

Exercise, a new study finds, changes the shape and functioning of our genes


http://well.blogs.nytimes.com/2014/12/17/how-exercise-changes-our-dna/?ref=health&_r=2

 

Gretchen Reynolds on the science of fitness.

We all know that exercise can make us fitter and reduce our risk for illnesses such as diabetes and heart disease. But just how, from start to finish, a run or a bike ride might translate into a healthier life has remained baffling.

Now new research reports that the answer may lie, in part, in our DNA. Exercise, a new study finds, changes the shape and functioning of our genes, an important stop on the way to improved health and fitness.

The human genome is astonishingly complex and dynamic, with genes constantly turning on or off, depending on what biochemical signals they receive from the body. When genes are turned on, they express proteins that prompt physiological responses elsewhere in the body.

Scientists know that certain genes become active or quieter as a result of exercise. But they hadn’t understood how those genes know how to respond to exercise.

Enter epigenetics, a process by which the operation of genes is changed, but not the DNA itself. Epigenetic changes occur on the outside of the gene, mainly through a process called methylation. In methylation, clusters of atoms, called methyl groups, attach to the outside of a gene like microscopic mollusks and make the gene more or less able to receive and respond to biochemical signals from the body.

Scientists know that methylation patterns change in response to lifestyle. Eating certain diets or being exposed to pollutants, for instance, can change methylation patterns on some of the genes in our DNA and affect what proteins those genes express. Depending on which genes are involved, it may also affect our health and risk for disease.

Far less has been known about exercise and methylation. A few small studies have found that a single bout of exercise leads to immediate changes in the methylation patterns of certain genes in muscle cells. But whether longer-term, regular physical training affects methylation, or how it does, has been unclear.

So for a study published this month in Epigenetics, scientists at the Karolinska Institute in Stockholm recruited 23 young and healthy men and women, brought them to the lab for a series of physical performance and medical tests, including a muscle biopsy, and then asked them to exercise half of their lower bodies for three months.

One of the obstacles in the past to precisely studying epigenetic changes has been that so many aspects of our lives affect our methylation patterns, making it difficult to isolate the effects of exercise from those of diet or other behaviors.

The Karolinska scientists overturned that obstacle by the simple expedient of having their volunteers bicycle using only one leg, leaving the other unexercised. In effect, each person became his or her own control group. Both legs would undergo methylation patterns influenced by his or her entire life; but only the pedaling leg would show changes related to exercise.

The volunteers pedaled one-legged at a moderate pace for 45 minutes, four times per week for three months. Then the scientists repeated the muscle biopsies and other tests with each volunteer.

Not surprisingly, the volunteers’ exercised leg was more powerful now than the other, showing that the exercise had resulted in physical improvements.

But the changes within the muscle cells’ DNA were more intriguing. Using sophisticated genomic analysis, the researchers determined that more than 5,000 sites on the genome of muscle cells from the exercised leg now featured new methylation patterns. Some showed more methyl groups; some fewer. But the changes were significant and not found in the unexercised leg.

Interestingly, many of the methylation changes were on portions of the genome known as enhancers that can amplify the expression of proteins by genes. And gene expression was noticeably increased or changed in thousands of the muscle-cell genes that the researchers studied.

Most of the genes in question are known to play a role in energy metabolism, insulin response and inflammation within muscles. In other words, they affect how healthy and fit our muscles — and bodies — become.

They were not changed in the unexercised leg.

The upshot is that scientists now better understand one more step in the complicated, multifaceted processes that make exercise so good for us.

Many mysteries still remain, though, said Malene Lindholm, a graduate student at the Karolinska Institute, who led the study. It’s unknown, for example, whether the genetic changes she and her colleagues observed would linger if someone quits exercising and how different amounts or different types of exercise might affect methylation patterns and gene expression. She and her colleagues hope to examine those questions in future studies.

But the message of this study is unambiguous. “Through endurance training — a lifestyle change that is easily available for most people and doesn’t cost much money,” Ms. Lindholm said, “we can induce changes that affect how we use our genes and, through that, get healthier and more functional muscles that ultimately improve our quality of life.”

 

Cholesterol & heart disease – there is a relationship, but it’s not what you think


http://pi-bill-articles.blogspot.com/2012/12/cholesterol-heart-disease-there-is.html?spref=tw

The serious bit
The WHO data is split into men and women. I first did the scatter diagrams for average (mean) cholesterol levels and CVD deaths. Then I ran the Pearson correlation coefficient on these numbers. This gives us the term called “r”. “r” tells us if there is some kind of a relationship: an r score of 0 would indicate no relationship; an r score of 1 would indicate a perfect relationship. A negative r score is called an inverse relationship e.g. the price of concert tickets is likely to be inversely related to the number of concert tickets bought – fewer tickets being bought at higher prices.

The “r” score for men revealed that there was a small relationship of 0.13 – however this relationship was inverse. The diagram and correlation shows that higher cholesterol levels are associated with lower CVD deaths and lower cholesterol levels are associated with higher CVD deaths. In women, the relationship is stronger – to the point of being meaningful. The r score was 0.52 – but, again, inverse. For women, higher cholesterol levels are quite significantly associated with lower CVD deaths and lower cholesterol levels are quite significantly associated with higher CVD deaths. Please note that I have added r squared on the graphs below (excel can do this for us) and it can confirm that you’ve got your r numbers right and r squared tells us the strength of any relationship we have observed.

All you need to do is to look at the lines going down to the right and wonder how on earth we ever got away with telling people that cholesterol causes heart disease. High cholesterol is associated with lower heart disease and vice versa – for all the data available in the world. High cholesterol is not even associated with high heart disease, let alone does it cause it.

Click the link and read this article. The charts show the higher the cholesterol, the lower heart disease is and the lower cholesterol, the higher heart disease goes.

Worth the read.

~tannngl

 

A beginning: ‘They’re’ going to tell us that eating cholesterol is ok…


http://www.washingtonpost.com/blogs/wonkblog/wp/2015/02/10/feds-poised-to-withdraw-longstanding-warnings-about-dietary-cholesterol/

The nation’s top nutrition advisory panel has decided to drop its caution about eating cholesterol-laden food, a move that could undo almost 40 years of government warnings about its consumption.

The group’s finding that cholesterol in the diet need no longer be considered a “nutrient of concern” stands in contrast to the committee’s findings five years ago, the last time it convened. During those proceedings, as in previous years, the panel deemed the issue of “excess dietary cholesterol” a public health concern. The most current finding was discussed at the group’s last meeting.

The new view on cholesterol in the diet does not reverse warnings about high levels of “bad” cholesterol in the blood, which have been linked to heart disease. Moreover, some experts warned that people with particular health problems, such as diabetes, should continue to avoid cholesterol-rich diets.

But the finding, which may offer a measure of relief to breakfast diners who prefer eggs, follows an evolution of thinking among many nutritionists who now believe that for a healthy adult cholesterol intake may not significantly affect the level of cholesterol in the blood or increase the risk of heart disease. The greater danger, according to this line of thought, lies in foods heavy with trans fats and saturated fats.

The panel laid out the cholesterol decision in December, at its last meeting before it writes a report that will serve as the basis for the next version of the “Dietary Guidelines,” a federal publication that has broad effects on the American diet. A video of the meeting was later posted online and a person with direct knowledge of the proceedings said the cholesterol finding would make it to the group’s final report, which is due within weeks.

After Marian Neuhouser, chair of the relevant subcommittee, announced the decision to the panel at the December meeting, one panelist appeared to bridle.

“So we’re not making a [cholesterol] recommendation?” panel member Miriam Nelson, a Tufts University professor, said at the meeting as if trying to absorb the thought. “Okay … Bummer.”

Members of the panel, called the Dietary Guidelines Advisory Committee, said they would not comment until the publication of their report.

You need to read this long article at the Washington Post.

Unbelievable. (Actually it’s believable-for as long as I’ve been a nurse, about 49 year,these changes in expert opinion occur at regular intervals.)

There really should be much more coming down the pike in dietary changes. But it will be slow. Don’t hold your breath.

~tannngl

Memory loss associated with Alzheimer’s reversed for the first time!


Small trial by UCLA and Buck Institute succeeds using ‘systems approach’ to memory disorders

 

http://newsroom.ucla.edu/releases/memory-loss-associated-with-alzheimers-reversed-for-first-time

 

Patient 1 had two years of progressive memory loss. She was considering quitting her job, which involved analyzing data and writing reports, she got disoriented driving, and she mixed up the names of her pets.

Patient 2 kept forgetting once-familiar faces at work, forgot his gym locker combination and had to have his assistants constantly remind him of his work schedule.

Patient 3’s memory was so bad that she used an iPad to record everything, then forgot her password. Her children noticed she commonly lost her train of thought in mid-sentence, and often asked them if they had carried out the tasks that she mistakenly thought she had asked them to do.

— “Reversal of cognitive decline: A novel therapeutic program,” UCLA/Buck Institute, 2014

Since it was first described over 100 years ago, Alzheimer’s disease has been without an effective treatment.

That may finally be about to change: In the first, small study of a novel, personalized and comprehensive program to reverse memory loss, nine of 10 participants, including those described above, displayed subjective or objective improvement in their memories beginning within three to six months.

Six patients had discontinued working or had been struggling at their jobs at the time they joined the study; all were able to return to their jobs or continue working with improved performance, and their improvements have been sustained. (The patient in treatment the longest has been receiving the therapy for two-and-a-half years.)

Among the 10 were patients with memory loss associated with Alzheimer’s disease, amnestic mild cognitive impairment or subjective cognitive impairment (in which the patient reports cognitive problems). One patient who had been diagnosed with late stage Alzheimer’s did not improve.

The study was conducted Dr. Dale Bredesen of the UCLA Mary S. Easton Center for Alzheimer’s Disease Research and the Buck Institute for Research on Aging. It is the first to suggest that memory loss in patients may be reversed — and improvement sustained — using a complex, 36-point therapeutic program that involves comprehensive diet changes, brain stimulation, exercise, sleep optimization, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry.

The findings are published in the current online edition of the journal Aging.

Bredesen, UCLA’s Augustus Rose Professor of Neurology, director of the Easton Center and the paper’s author, said the findings are “very encouraging,” but he added that the results are anecdotal, and a more extensive, controlled clinical trial is needed.

No single drug has been found to stop or even slow the progression of Alzheimer’s, and drugs have only had modest effects on symptoms. “In the past decade alone, hundreds of clinical trials have been conducted for Alzheimer’s, without success, at an aggregate cost of over $1 billion,” said Bredesen, who also is a professor at the Buck Institute.

Although other chronic illnesses such as cardiovascular disease, cancer and HIV have been improved through the use of combination therapies, comprehensive combination therapies have not been explored for Alzheimer’s and other memory disorders. However, over the past few decades, genetic and biochemical research has revealed an extensive network of molecular interactions involved in the development of Alzheimer’s.

“That suggested that a broader-based therapeutic approach, rather than a single drug that aims at a single target, may be feasible and potentially more effective for the treatment of cognitive decline due to Alzheimer’s,” Bredesen said.

While extensive preclinical studies in numerous other laboratories have identified single pathogenic targets for potential intervention, in human studies, such single target therapeutic approaches have not borne out. But, said Bredesen, it’s possible that addressing multiple targets within the network underlying Alzheimer’s may be successful even when each target is affected in a relatively modest way. “In other words,” he said, “the effects of the various targets may be additive, or even synergistic.”

The uniform failure of drug trials in Alzheimer’s influenced Bredesen’s desire to better understand the fundamental nature of the disease. His laboratory has found evidence that Alzheimer’s stems from an imbalance in nerve cell signaling. In the normal brain, specific signals foster nerve connections and memory making, while balancing signals support memory loss, allowing irrelevant information to be forgotten. But in people with Alzheimer’s, the balance of these opposing signals is disturbed, nerve connections are suppressed and memories are lost.

That finding is contrary to the popular belief that Alzheimer’s is caused by the accumulation of sticky plaques in the brain. Bredesen believes the amyloid beta peptide, the source of the plaques, has a normal function in the brain, as part of a larger set of molecules that promote signals that cause nerve connections to lapse. Thus, the increase in the peptide that occurs in Alzheimer’s shifts the balance in favor of memory loss.

Bredesen therefore thought that, rather than a single targeted agent, the solution might be a multiple-component system approach, in line with the approach for other chronic illnesses.

“The existing Alzheimer’s drugs affect a single target, but Alzheimer’s disease is more complex. Imagine having a roof with 36 holes in it, and your drug patched one hole very well,” he said. “The drug may have worked, and a single hole may have been fixed, but you still have 35 other leaks, and so the underlying process may not be affected much.”

Bredesen’s approach is personalized to the patient, based on extensive testing to determine what is affecting the brain’s plasticity signaling network. In the case of the patient with the demanding job who was forgetting her way home, her therapy consisted of some, but not all, of the components of Bredesen’s program, including:

eliminating all simple carbohydrates, gluten and processed food from her diet, and eating more vegetables, fruits and non-farmed fish
meditating twice a day and beginning yoga to reduce stress
sleeping seven to eight hours per night, up from four to five
taking melatonin, methylcobalamin, vitamin D3, fish oil and coenzyme Q10 each day
optimizing oral hygiene using an electric flosser and electric toothbrush
reinstating hormone replacement therapy, which had previously been discontinued
fasting for a minimum of 12 hours between dinner and breakfast, and for a minimum of three hours between dinner and bedtime
exercising for a minimum of 30 minutes, four to six days per week
Bredesen said the program’s downsides are its complexity and that the burden falls on patients and caregivers to follow it. In the study, none of the patients was able to stick to the entire protocol. Their most common complaints were the diet and lifestyle changes, and having to take multiple pills each day.

The good news, though, said Bredesen, are the side effects: “It is noteworthy that the major side effects of this therapeutic system are improved health and an improved body mass index, a stark contrast to the side effects of many drugs.”

The results suggest that memory loss may be reversed and improvement sustained with the therapeutic program, but Bredesen cautioned that the results need to be replicated.

“The current, anecdotal results require a larger trial, not only to confirm or refute the results reported here, but also to address key questions raised, such as the degree of improvement that can be achieved routinely, how late in the course of cognitive decline reversal can be effected, whether such an approach may be effective in patients with familial Alzheimer’s disease, and last, how long improvement can be sustained,” he said.

Cognitive decline is a major concern of the aging population. Alzheimer’s affects approximately 5.4 million Americans and 30 million people globally. By 2050, without effective prevention and treatment, an estimated 160 million people globally would have the disease, including 13 million Americans, which could potentially bankrupt the Medicare system. Unlike several other chronic illnesses, the incidence of Alzheimer’s is on the rise; recent estimates suggest that it has become the third leading cause of death in the U.S. behind cardiovascular disease and cancer.

Multiple entities provided support for the study, including the National Institutes of Health (AG16570, AG034427 and AG036975). The complete list is included in the paper.