From Colin Champ, MD’s blog:
Several years back a scientific article revealed that those of us with high “muscular strength” have a lower risk of becoming a victim to cancer – a 40% lower risk to be exact.1 After assessment of almost 9,000 men aged 20-82, scientists found that men with a stronger one-rep max on bench press and leg press have a 40% reduction in their risk of dying from cancer. They adjusted for body mass index (BMI), body fat, and cardiorespiratory fitness and the results still held strong (pun intended).2 In other words, there is something about simply being stronger that can lower our risk of getting cancer. Many felt as though there was something innately healthy about having more muscles, but another study associated weak hand grip strength with an increased risk of cancer, even regardless of muscle size.3 So is it all about strength or do muscles fight cancer?
Strength goes beyond lowering our risk of dying from cancer; it lowers our risk of dying from most major health issues. For instance, men exhibiting a lower vertical leap, less sit-ups, and decreased grip strength have a higher risk of dying period.4 Men and women with moderate and high bench press and sit-up scores have lower risks of death,5 while men with a higher 1-repetition bench and leg press apparently live longer (even when we account for other health issues, like cardiovascular disease, smoking, obesity, etc.).6
Muscles Fight Cancer – More Muscles = More Health?
The first thought that comes to mind is that more muscles means more strength, and both are a result of more exercise. Sure enough, when we take a close look through these studies, we do see that the strongest among us have less body fat, are in better shape, and have better “good” cholesterol values with lower blood sugar and triglycerides.1 This is not surprising.
However, in nearly all these “muscles fight cancer” studies, other health issues were adjusted for and the findings still held. In other words, these studies seem to suggest that strength is independently associated with a lower risk of cancer and a higher change of avoiding an untimely death, regardless of age, smoking, alcohol usage, or other health issues. But as we know, associations can only take us so far, before we must explore the mechanism that support these associations.
Muscles Fight Cancer – It’s the Muscles!
In the study above, the scientists found some intriguing results: the benefits of muscular strength overlap with cardiovascular fitness, but the benefits of muscular strength in decreasing the risk of cancer death work through different mechanisms.1 Perhaps the synergy exists, or in other words, having more muscle and strength is good, and exercising them is better.
For instance, we know that exercising our muscles leads to:
Improved insulin sensitivity (less insulin needed to remove sugar from our blood)
More sugar extracted from our blood by skeletal muscle and used for energy during exercise
Less cancer-promoting sugar and insulin floating around our blood
A decrease in the levels of hormones that, over a prolonged period, can lead to cancer. For instance, resistance training increases IGFBP-3, which binds to insulin-like growth factor (IGF), decreasing its ability to promote cancer (growth factors are normal within the human body, but too many can lead to excessive cellular growth, including cancer growth)7
Decreased inflammation (which when present, serves as a fertilizer for cancer)
Increased antioxidant defense, which helps fight potential cancer-causing free-radicals
Less inflammation-producing body fat
However, recent studies have changed much of our thinking when it comes to muscle. There are many organs in our body that respond to stimuli and secrete hormones, which serve as messages to direct remote parts of the body. We are recently starting to find some more unconventional organ-like structures in the body. For instance, it is now well-established that our adipose tissue works like an endocrine organ – albeit a bad one – secreting inflammatory hormones and an excess of potentially cancer-stimulating hormones.8 Take estrogen for example, which is a hormone that both men and women require to function normally. However, when supplied in higher than physiologically normal amounts from excess body fat, it can increase a woman’s risk of breast cancer. When women lose theses additional pounds through dietary changes and exercise, estrogen levels decrease.9
Studies have now shown that fat is not the only recently discovered endocrine organ. Muscle may act similarly, though this time to the benefit of our health. The metabolic muscular organ within us secretes IL-6, an important cytokine that was once felt to be a bad guy that caused inflammation. Newer studies reveal that IL-6 has a healthy role and is actually a myokine, which is an endocrine hormone produced by muscle (myo = muscle) and released during contraction. In other words, while fat secretes harmful hormones, muscles squeeze out some healthy hormones during lifting.
You can read the rest at his site referenced above. He is a radiation oncologist and stays up on what’s new in cancer and ways we can fight this disease.
He gives us the Warburg effect from the early 1900’s. These things decrease cancer and its hold on us.:
Muscle contraction during exercise,16,17 with the more intense exercise resulting in increased expression of AMPK18
Carbohydrate restriction (with or without fasting and even in the face of an increase in calories)19
There is much on complex chemical processes in our bodies and how these all work together to make us healthy or sick. Good article on muscles making us fight cancer!!
As scientists learn more about the key role of inflammation in diabetes, heart disease and other disorders, new research from Washington University School of Medicine in St. Louis suggests that fat in the belly may be an important promoter of that inflammation.
In this abdominal MRI scan, it is possible to see subcutaneous fat around the abdomen, surrounding
In this abdominal MRI scan, it is possible to see subcutaneous fat around the abdomen, surrounding abdominal muscles. Visceral fat is deeper inside the abdomen, surrounding internal organs.It is the visceral fat that secretes IL-6, strongly suggesting a mechanistic link to systemic inflammation.
Excess fat is known to be associated with disease, but now the researchers have confirmed that fat cells inside the abdomen are secreting molecules that increase inflammation. It’s the first evidence of a potential mechanistic link between abdominal fat and systemic inflammation.
For years, scientists have been aware of a relationship between disease risk and excess belly fat. “Apple-shaped” people, who carry fat in the abdomen, have a higher risk of heart disease, diabetes and other problems than “pear-shaped” people, who tend to store fat in the hips and thighs. Too much abdominal fat is associated with a defect in the body’s response to insulin. During medical exams, some physicians measure waist circumference to identify patients at increased risk for these problems.
Not just any belly fat will cause inflammation, however. Back in 2004, Washington University investigators found that removing abdominal fat with liposuction did not provide the metabolic benefits normally associated with similar amounts of fat loss induced by dieting or exercising.
“Despite removing large amounts of subcutaneous fat from beneath the skin — about 20 percent of a person’s total body fat mass — there were no beneficial medical effects,” says Samuel Klein, M.D., the Danforth Professor of Medicine and Nutritional Science and the senior investigator on both studies. “These results demonstrated that decreasing fat mass by surgery, which removes billions of fat cells, does not provide the metabolic benefits seen when fat mass is reduced by lowering calorie intake, which shrinks the size of fat cells and decreases the amount of fat inside the abdomen and other tissues.”
In this new study, researchers looked instead at visceral fat — the fat that surrounds the organs in the gut. Unlike subcutaneous fat, visceral fat is not easy to remove surgically because it is very close to the intestines and other internal organs. Since they couldn’t just take out the fat, the research team decided to analyze the blood that ran through it to determine whether visceral fat was involved in inflammation or whether, like subcutaneous fat, it was merely a marker of potential problems.
Reporting in the journal Diabetes, the research team says visceral fat likely contributes to increases in systemic inflammation and insulin resistance. They sampled blood from the portal vein in obese patients undergoing gastric bypass surgery and found that visceral fat in the abdomen was secreting high levels of an important inflammatory molecule called interleukin-6 (IL-6) into portal vein blood.
“The portal vein is filled with blood that drains visceral fat,” says first author Luigi Fontana, M.D., Ph.D., assistant professor of medicine at Washington University in St. Louis and an investigator at the Istituto Superiore di Sanita, Rome, Italy. “Portal vein blood had levels of IL-6 that were 50 percent higher than blood from the periphery.”
Increased IL-6 levels in the portal vein correlated with concentrations of an inflammatory substance called C-reactive protein (CRP) in the body. High CRP levels are related to inflammation, and chronic inflammation is associated with insulin resistance, hypertension, type 2 diabetes and atherosclerosis, among other things.
“These data support the notion that visceral fat produces inflammatory cytokines that contribute to insulin resistance and cardiovascular disease,” says Klein.
Klein, Fontana and J. Christopher Eagon, M.D., assistant professor of surgery, looked at blood samples from 25 patients. All were extremely obese, and all were undergoing gastric bypass surgery. They took blood from the portal vein and from the radial artery in the arm and found differences in levels of IL-6 between the samples.
Fontana believes the findings help explain how visceral fat can lead to inflammation, insulin resistance and other metabolic problems. And he says by contributing to inflammation, visceral fat cells in the abdomen may be doing even more than that.
“Many years ago, atherosclerosis was thought to be related to lipids and to the excessive deposit of cholesterol in the arteries,” Fontana says. “Nowadays, it’s clear that atherosclerosis is an inflammatory disease. There also is evidence that inflammation plays a role in cancer, and there is even evidence that it plays a role in aging. Someday we may learn that visceral fat is involved in those things, too.”
Fontana L, Eagon JC, Trujillo ME, Scherer PE, Klein S. Visceral fat adipokine secretion is associated with systemic inflammation in obese humans. Diabetes, published online Feb. 7, 2007.
This research was supported by grants from the National Institutes of Health.
Washington University School of Medicine’s full-time and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children’s hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked fourth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children’s hospitals, the School of Medicine is linked to BJC HealthCare.
The strongly-worded editorial in the British Journal of Sports Medicine, published in the May edition of the journal, says you can’t outrun a bad diet and that although regular exercise reduces the risk of developing a number of health issues such as heart disease, dementia, some cancers and type 2 diabetes, it doesn’t promote weight loss unless it is paired with dietary changes.
Worldwide obesity has doubled since 1980, according to the World Health Organization, with 600 million people globally categorised as obese. In the UK obesity affects one in four adults, according to the NHS.
The NHS defines obesity as adults who have a Body Mass Index of 30 or over.
The authors of the study say the public is “drowned by an unhelpful message” from the food industry that obesity is caused entirely by a lack of exercise, going so far as to describe the tactics used as “chillingly similar” to those employed by big tobacco companies when the links between smoking and lung cancer were first revealed.
“The tobacco industry successfully stalled government intervention for 50 years,” they say. “This sabotage was achieved using a ‘corporate playbook’ of denial, doubt, confusing the public and even buying the loyalty of bent scientists, at the cost of millions of lives.”
Study takes aim at sugary drinks.
The food industry has also shifted the conversation to simple calorie counting, the authors write. But it’s the source of calories that matters, the editorial says, arguing that sugar calories promote the storage of fat and make people more hungry, while calories that actually come from fat make a person feel full.
The authors point to a study in the academic journal Nutrition that says the single most effective way to counter obesity is to restrict the intake of carbohydrates.
The editorial also strongly criticises sugary drinks, saying the association between “junk food and sport, must end.” It calls on the British government to put a tax on sugary drinks and ban the advertising of junk food as well as saying gyms shouldn’t sell the beverages.
In a statement emailed to Mashable, Britain’s Food and Drink Federation strongly rejected comparisons with the tobacco industry, calling them “absurd and offensive” Britain’s Food and Drink Federation strongly rejected comparisons with the tobacco industry, calling them “absurd and offensive”.
“Britain’s food and drink manufacturers are proud of their long track record of working to help improve UK diets and promote healthier lifestyles. But they’re not complacent, recognising the scale of the obesity challenge in the UK,” the statement says, pointing to the introduction nutrition information on food packaging and a push towards a reduction of salt usage.
It says that the benefits of exercise aren’t industry hype or conspiracy.
“Yes, companies are taking action to highlight the importance of physical activity. However, they recognise that where they can have the biggest impact is in helping people to achieve a balanced diet,” they say.
The NHS currently advises that people trying to lose weight should eat a balanced, calorie controlled diet and take up activities such as fast walking, jogging, swimming or tennis for up to 300 minutes per week.
Weights keep brain nimble, research suggests
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.
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.”
Click on this URL for this Healthwire.com article:
I have pasted the last half of this article here. Please visit the above site for this cell biology information on cutting of food to cancer cells!
Fasting, the Ketogenic Diet and AMP-K: The New Kid on the Block
AMPK and Warburg
The Warburg hypothesis is something that comes up often around these parts. Very briefly put, Warburg showed that whether oxygen was present or not, cancer cells would rather use glucose for energy derivation. Even though when oxygen is present, cells can rely on mitochondria to make significantly more energy, cancer cells still seem to rely on the inefficient process of glycolysis (the breakdown of sugar).Well, while AMPK may stop cancer by blocking pathways like mTOR, newer data shows that it actually blocks the Warburg Effect by blocking the ability of cancer cells to use sugar for energy.4
Amping up AMPK
The great thing about AMPK, is the plethora of ways we seem to be able to manipulate it. AmpK seems to take away the helplessness of disease or “luck” of cancer and lets us know that we do have biologic pathways that can clearly be manipulated by our lifestyle to thwart off disease.
AMPK is upregulated via several mechanisms (in no apparent order):
Muscle contraction during exercise,5,6 with the more intense exercise resulting in increased expression of AMPK7
Carbohydrate restriction (with or without fasting and even in the face of an increase in calories)8
In a very nerdy, sciency kind of way, AMPK is one of the many reasons why the current and ancient lifestyle that relies on lower amounts of carbohydrates in the diet along with periodic lifting of heavy weights and intense exercise like sprinting puts so many people back in control of their health and in the driver’s seat in the fight against cancer. Activation of AMPK, which we can directly affect through our actions, may be putting us in an enhanced metabolic state to fight disease.
Summing it up
With all the recent talk of fasting, a ketogenic diet, and even calorie restriction, insulin (the hormone raised after carbohydrates are consumed in the diet) and the insulin-like growth factor receptor (where insulin and IGF bind) have been getting most of the hype. While it is well-deserved, as they are heavily implicated in cancer diagnosis and progression, we seem to be forgetting about AMPK, the new kid on the block. If we can increase an enzyme that helps stop cancer by fasting, limited carbs, and lifting some weights, isn’t the effect of lifestyle on health common sense at this point?
And remember, even biochemically and metabolically, our lifestyles and actions translate to our health. While Milli Vanilli may not, AMPK helps prove this.