DARWIN isn’t required reading for public health officials, but he should be. One reason that heart disease, diabetes and obesity have reached epidemic levels in the developed world is that our modern way of life is radically different from the hunter-gatherer environments in which our bodies evolved. But which modern changes are causing the most harm?
Many in public health believe that a major culprit is our sedentary lifestyle. Faced with relatively few physical demands today, our bodies burn fewer calories than they evolved to consume — and those unspent calories pile up over time as fat. The World Health Organization, in discussing the root causes of obesity, has cited a “decrease in physical activity due to the increasingly sedentary nature of many forms of work, changing modes of transportation and increasing urbanization.” This is a nice theory. But is it true? To find out, my colleagues and I recently measured daily energy expenditure among the Hadza people of Tanzania, one of the few remaining populations of traditional hunter-gatherers. Would the Hadza, whose basic way of life is so similar to that of our distant ancestors, expend more energy than we do? Our findings, published last month in the journal PLoS ONE, indicate that they don’t, suggesting that inactivity is not the source of modern obesity. Previous attempts to quantify daily energy expenditure among hunter-gatherers have relied entirely on estimation. By contrast, our study used a technique that calculates the body’s rate of carbon dioxide production — and hence the calories burned per day — by tracking the depletion of two isotopes (deuterium and oxygen-18) in an individual’s urine over a two-week period. It was a testament to the Hadza’s graciousness, and their years of friendship with several of my colleagues, that they welcomed us into their camps and participated in the study. As we sat back and observed, the Hadza went about their normal routines. The Hadza live in simple grass huts in the middle of a dry East African savanna. They have no guns, vehicles, crops or livestock. Each day the women comb miles of hilly terrain, foraging for tubers, berries and other wild plant foods, often while carrying infants, firewood and water. Men set out alone most days to collect honey or hunt for game using handmade bows and poison-tipped arrows, often covering 15 to 20 miles. We found that despite all this physical activity, the number of calories that the Hadza burned per day was indistinguishable from that of typical adults in Europe and the United States. We ran a number of statistical tests, accounting for body mass, lean body mass, age, sex and fat mass, and still found no difference in daily energy expenditure between the Hadza and their Western counterparts. How can the Hadza be more active than we are without burning more calories? It’s not that their bodies are more efficient, allowing them to do more with less: separate measurements showed that the Hadza burn just as many calories while walking or resting as Westerners do. We think that the Hadzas’ bodies have adjusted to the higher activity levels required for hunting and gathering by spending less energy elsewhere. Even for very active people, physical activity accounts for only a small portion of daily energy expenditure; most energy is spent behind the scenes on the myriad unseen tasks that keep our cells humming and our support systems working. If the Hadza’s bodies somehow manage to spend less energy in those areas, they could easily accommodate the elevated energy demands of hunting and gathering. And indeed, studies reporting differences in metabolic-hormone profiles between traditional and Western populations support this idea (though more work is needed). Our findings add to a growing body of evidence suggesting that energy expenditure is consistent across a broad range of lifestyles and cultures. Of course, if we push our bodies hard enough, we can increase our energy expenditure, at least in the short term. But our bodies are complex, dynamic machines, shaped over millions of years of evolution in environments where resources were usually limited; our bodies adapt to our daily routines and find ways to keep overall energy expenditure in check. All of this means that if we want to end obesity, we need to focus on our diet and reduce the number of calories we eat, particularly the sugars our primate brains have evolved to love. We’re getting fat because we eat too much, not because we’re sedentary. Physical activity is very important for maintaining physical and mental health, but we aren’t going to Jazzercise our way out of the obesity epidemic. We have a lot more to learn from groups like the Hadza, among whom obesity and heart disease are unheard of and 80-year-old grandmothers are strong and vital. Finding new approaches to public health problems will require further research into other cultures and our evolutionary past. Source: http://mobile.nytimes.com/2012/08/26/opinion/sunday/debunking-the-hunter-gatherer-workout.html?_r=0&referer
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When I was growing up in the 80s, New Kids on the Block were a massive hit. Yet, I never understood why, nor was I interested in their music. With behemoths like Michael Jackson and Milli Vanilli, who had time for NKOTB? In fact, I even saw Milli Vanilli live in concert and it was definitely one of my fondest childhood memories.
Granted, they were lip-syncing everything, but when you are 10 years old and a concert starts out with Rob and Fab battling in a sword fight, it is hard to get more exciting than that... With all the recent focus on carbohydrates in the diet and blood sugar, insulin, and the insulin receptor (the Fab Morvan, Rob Pilatus, and Michael Jackson of the metabolic world) the new kid on the block seems to be AMPK. AMPK, or AMP-activated protein kinase, is an enzyme extensively expressed in our skeletal muscle, liver, and brain. It serves as an energy regulator and this function is in response to several dietary and lifestyle habits. Amping up AMPK AMPK is basically an energy sensor that gets enhanced when our ATP is reduced (think of ATP as a transporter of energy) and AMP increases. ATP has three phosphates (the T is for tri) and when it loses one becomes ADP (the D is for di, or two) and when it loses two phosphates it becomes AMP (the M is mono for one). Without going too chemistry class on the reader, it can be simply viewed as: ATP → ADP + P ATP → AMP + 2P AMPK works to bring that AMP back up to ATP. In other words, AMPK acts to increase our available energy molecules. AMPK achieves this through several mechanisms described in the pictorial below. The dark blue mechanisms involve breaking down glucose (sugar) to burn for energy. This can be done by pulling glucose out of our bloodstream and placing it into our cells to be consumed. The aqua circles represent the breaking down of cholesterol and fat to be used as an efficient source of energy. The purple includes building more mitochondria to use these fats and sugars to make more energy, and the light blue mechanisms turn off cell building and replication. Basically, AMPK signals to our bodies and cells that it is not a time for building, but rather for breaking down and burning. AMPK and Cancer: AMPK is in essence the antithesis of cancer. While cancer cells are burning large amounts of glucose and nutrients, this is mostly to build up biomass — or, simply put, to keep growing and spreading. AMPK, on the other hand, shuts off this process, blocking cancer growth so we can feed our own cells.1,2 As you can see in the picture below, AMPK actually blocks mTOR, a pathway that leads to cancer survival and growth.3 This is the same pathway that is blocked with targeted cancer drugs. You will also notice in this picture that the pathways are all affected by intermittent fasting, labeled as “IF.” You may also notice that increased insulin sensitivity, which happens though exercise and a healthy diet, also appears to upregulate AMPK. 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):
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. References: 1. Shackelford DB, Shaw RJ. The LKB1-AMPK pathway: metabolism and growth control in tumour suppression. Nat Rev Cancer. 2009;9(8):563-575. doi:nrc2676 [pii] 10.1038/nrc2676. 2. Green AS, Chapuis N, Maciel TT, et al. The LKB1/AMPK signaling pathway has tumor suppressor activity in acute myeloid leukemia through the repression of mTOR-dependent oncogenic mRNA translation. Blood. 2010;116(20):4262-4273. doi:blood-2010-02-269837 [pii] 10.1182/blood-2010-02-269837. 3. Champ CE, Baserga R, Mishra M V, et al. Nutrient Restriction and Radiation Therapy for Cancer Treatment: When Less Is More. Oncologist. 2013;18(1):97-103. doi:10.1634/theoncologist.2012-0164. 4. Faubert B, Boily G, Izreig S, et al. AMPK is a negative regulator of the Warburg effect and suppresses tumor growth in vivo. Cell Metab. 2013;17(1):113-124. doi:10.1016/j.cmet.2012.12.001. 5. Vavvas D, Apazidis A, Saha AK, et al. Contraction-induced changes in acetyl-CoA carboxylase and 5’-AMP-activated kinase in skeletal muscle. J Biol Chem. 1997;272(20):13255-13261. http://www.ncbi.nlm.nih.gov/pubmed/9148944. Accessed January 16, 2015. 6. Winder WW, Hardie DG. Inactivation of acetyl-CoA carboxylase and activation of AMP-activated protein kinase in muscle during exercise. Am J Physiol. 1996;270(2 Pt 1):E299-E304. http://www.ncbi.nlm.nih.gov/pubmed/8779952. Accessed January 16, 2015. 7. Rasmussen BB, Winder WW. Effect of exercise intensity on skeletal muscle malonyl-CoA and acetyl-CoA carboxylase. J Appl Physiol. 1997;83(4):1104-1109. http://www.ncbi.nlm.nih.gov/pubmed/9338417. Accessed January 16, 2015. 8. Draznin B, Wang C, Adochio R, Leitner JW, Cornier MA. Effect of Dietary Macronutrient Composition on AMPK and SIRT1 Expression and Activity in Human Skeletal Muscle. Horm Metab Res. 2012;44(09):650-655. doi:10.1055/s-0032-1312656. 9. Cantó C, Jiang LQ, Deshmukh AS, et al. Interdependence of AMPK and SIRT1 for metabolic adaptation to fasting and exercise in skeletal muscle. Cell Metab. 2010;11(3):213-219. doi:10.1016/j.cmet.2010.02.006. Source: http://www.myhealthwire.com/news/herbs-supplements/963 During the years I practised as a hospital doctor I saw only one amputee. He’d had his lower leg amputated for bad circulation worsened by smoking . He wouldn’t give up his Woodbines, though, not even if his other leg was in jeopardy.
It’s a totally different picture today. Amputation is becoming commonplace – as a complication of diabetes. And no one seems worried. That’s because so many people are obese and it’s accepted as normal. Fat people develop Type 2 diabetes, and that, in turn, has become ‘normal’. People with Type 2 diabetes develop gangrene which often requires amputation and even that’s ‘normal’. Except it isn’t. Diabetes is perpetually in the news. It costs £10billion a year, a tenth of the total NHS budget. Britain now has an estimated four million diabetics, and many are undiagnosed. I find the lack of discussion about the consequences of diabetes terrifying. It has no cure and if it’s ignored, it will get worse. In Britain, diabetes causes 7,000 amputations a year – 135 legs are cut off every week and rising. Diabetes is nothing if not aggressive. It hurts every organ in the body. High blood sugar levels damage the delicate lining of small arteries leading to restriction of circulation to the legs. You lose sensation in your feet so if you stand on a pin, you won’t feel it. Infections are more virulent and poor circulation means antibiotics can’t reach the infection and amputation follows. According to Diabetes UK, 80% of amputations could be prevented. Dr Natasha Patel is a consultant in diabetes at Guy’s and St Thomas’ hospitals and says Type 2 patients often go into denial. They ignore advice and don’t take their medication. Guy’s and St Thomas’ vascular surgeon, Hany Zayed, is able to salvage many legs by bypassing a blockage or inserting a stent to keep blood flowing. But often, as the disease progresses, a blockage will occur again elsewhere. Often it’s a leg or a life, he says. For Zayed, an amputation is a failure. The key to surviving diabetes, he says, is “taking ownership of your health”. But most of his patients don’t look after themselves. Worse still, they ignore a foot infection after they’ve lost all feeling. Diabetics must check their feet daily, not walk barefoot, avoid ill-fitting shoes and get someone to cut their toenails. Zayed hates performing amputations. “It’s awful,” he says. “I have been trained for 20 years to save lives and legs.” http://www.mirror.co.uk/lifestyle/health/obesity-crisis-fuelling-rise-amputations-8083485 An impressive lecture about cannabis but with several references to cannabidiol and dietary modulators of the endocannabinoid system. He briefly discusses his 2004 theory of ECS dysfunction causing disease and provides evidence of ECS connection to common painful connections. Of special interest are pre & pro-biotics and foods shown to be effective in disease conditions and modulating the ECS. Many more lectures in this recent series. He also offers to share his information without restrictions including his upcoming comprehensive cannabis review article.. Click here to Make your own, heathy version of candies.
Chocolate Peanut Butter Cups from All Day I Dream About Food Mock Payday Bars from Healthy Indulgences Coconut Chocolate Bars from The Nourished Caveman Sugar-Free Twix from All Day I Dream About Food Copycat Ferrero Rocher from Sugar Free Mom Bourbon Chocolate Truffles from I Breathe, I’m Hungry Sugar-Free Gummy Candies from Whole New Mom Better Than Mounds Chocolate Coconut Candies from All Day I Dream About Food Turtles from Maria Mind Body Health Keto Peppermint Patties from Worth Every Chew Sugar-Free Cream Cheese Candies from Low Carb So Simple Dark Chocolate Sea Salt Almond Bark from All Day I Dream About Food Low Carb Chocolate Coconut Fat Bombs from Grassfed Girl Toasted Coconut Butter Cups from Holistically Engineered Low Carb Marshmallows from Keto Diet Blog Whatchamacallit Bars from All Day I Dream About Food White Chocolate Pecan Bark from Carb Wars Pumpkin Fudge from The Coers Family Keto Choconut Almond Butter Cups from The Healthy Foodie Maple Walnut Candy from All Day I Dream About Food Butter Pecan Fat Bombs from Fluffy Chix Cook Strawberry Peeps Fat Bombs from Up Late Anyway Salted Peanut Caramel Clusters from All Day I Dream About Food Snickers Candy Bars from Maria Mind Body Health Lemon Lime Coconut Candies from Delicious Obsessions Salted Caramel Cake Pops from All Day I Dream About Food Reese’s Fudge from Desserts With Benefits Keto Coconut Fat Bombs from Keto Diet Blog Bulletproof Coffee Gummies from Cheerfully Imperfect edit. In the early 20th century, the German biochemist Otto Warburg believed that tumors could be treated by disrupting their source
of energy. His idea was dismissed for decades — until now. The story of modern cancer research begins, somewhat improbably, with the sea urchin. In the first decade of the 20th century, the German biologist Theodor Boveri discovered that if he fertilized sea-urchin eggs with two sperm rather than one, some of the cells would end up with the wrong number of chromosomes and fail to develop properly. It was the era before modern genetics, but Boveri was aware that cancer cells, like the deformed sea urchin cells, had abnormal chromosomes; whatever caused cancer, he surmised, had something to do with chromosomes. Today Boveri is celebrated for discovering the origins of cancer, but another German scientist, Otto Warburg, was studying sea-urchin eggs around the same time as Boveri. His research, too, was hailed as a major breakthrough in our understanding of cancer. But in the following decades, Warburg’s discovery would largely disappear from the cancer narrative, his contributions considered so negligible that they were left out of textbooks altogether. Unlike Boveri, Warburg wasn’t interested in the chromosomes of sea-urchin eggs. Rather, Warburg was focused on energy, specifically on how the eggs fueled their growth. By the time Warburg turned his attention from sea-urchin cells to the cells of a rat tumor, in 1923, he knew that sea-urchin eggs increased their oxygen consumption significantly as they grew, so he expected to see a similar need for extra oxygen in the rat tumor. Instead, the cancer cells fueled their growth by swallowing up enormous amounts of glucose (blood sugar) and breaking it down without oxygen. The result made no sense. Oxygen-fueled reactions are a much more efficient way of turning food into energy, and there was plenty of oxygen available for the cancer cells to use. But when Warburg tested additional tumors, including ones from humans, he saw the same effect every time. The cancer cells were ravenous for glucose. Warburg’s discovery, later named the Warburg effect, is estimated to occur in up to 80 percent of cancers. It is so fundamental to most cancers that a positron emission tomography (PET) scan, which has emerged as an important tool in the staging and diagnosis of cancer, works simply by revealing the places in the body where cells are consuming extra glucose. In many cases, the more glucose a tumor consumes, the worse a patient’s prognosis. In the years following his breakthrough, Warburg became convinced that the Warburg effect occurs because cells are unable to use oxygen properly and that this damaged respiration is, in effect, the starting point of cancer. Well into the 1950s, this theory — which Warburg believed in until his death in 1970 but never proved — remained an important subject of debate within the field. And then, more quickly than anyone could have anticipated, the debate ended. In 1953, James Watson and Francis Crick pieced together the structure of the DNA molecule and set the stage for the triumph of molecular biology’s gene-centered approach to cancer. In the following decades, scientists came to regard cancer as a disease governed by mutated genes, which drive cells into a state of relentless division and proliferation. The metabolic catalysts that Warburg spent his career analyzing began to be referred to as “housekeeping enzymes” — necessary to keep a cell going but largely irrelevant to the deeper story of cancer. The Health Issue “It was a stampede,” says Thomas Seyfried, a biologist at Boston College, of the move to molecular biology. “Warburg was dropped like a hot potato.” There was every reason to think that Warburg would remain at best a footnote in the history of cancer research. (As Dominic D’Agostino, an associate professor at the University of South Florida Morsani College of Medicine, told me, “The book that my students have to use for their cancer biology course has no mention of cancer metabolism.”) But over the past decade, and the past five years in particular, something unexpected happened: Those housekeeping enzymes have again become one of the most promising areas of cancer research. Scientists now wonder if metabolism could prove to be the long-sought “Achilles’ heel” of cancer, a common weak point in a disease that manifests itself in so many different forms. There are typically many mutations in a single cancer. But there are a limited number of ways that the body can produce energy and support rapid growth. Cancer cells rely on these fuels in a way that healthy cells don’t. The hope of scientists at the forefront of the Warburg revival is that they will be able to slow — or even stop — tumors by disrupting one or more of the many chemical reactions a cell uses to proliferate, and, in the process, starve cancer cells of the nutrients they desperately need to grow. Advertisement Even James Watson, one of the fathers of molecular biology, is convinced that targeting metabolism is a more promising avenue in current cancer research than gene-centered approaches. At his office at the Cold Spring Harbor Laboratory in Long Island, Watson, 88, sat beneath one of the original sketches of the DNA molecule and told me that locating the genes that cause cancer has been “remarkably unhelpful” — the belief that sequencing your DNA is going to extend your life “a cruel illusion.” If he were going into cancer research today, Watson said, he would study biochemistry rather than molecular biology. “I never thought, until about two months ago, I’d ever have to learn the Krebs cycle,” he said, referring to the reactions, familiar to most high-school biology students, by which a cell powers itself. “Now I realize I have to.” Born in 1883 into the illustrious Warburg family, Otto Warburg was raised to be a science prodigy. His father, Emil, was one of Germany’s leading physicists, and many of the world’s greatest physicists and chemists, including Albert Einstein and Max Planck, were friends of the family. (When Warburg enlisted in the military during World War I, Einstein sent him a letter urging him to come home for the sake of science.) Those men had explained the mysteries of the universe with a handful of fundamental laws, and the young Warburg came to believe he could bring that same elegant simplicity and clarity to the workings of life. Long before his death, Warburg was considered perhaps the greatest biochemist of the 20th century, a man whose research was vital to our understanding not only of cancer but also of respiration and photosynthesis. In 1931 he won the Nobel Prize for his work on respiration, and he was considered for the award on two other occasions — each time for a different discovery. Records indicate that he would have won in 1944, had the Nazis not forbidden the acceptance of the Nobel by German citizens. That Warburg was able to live in Germany and continue his research throughout World War II, despite having Jewish ancestry and most likely being gay, speaks to the German obsession with cancer in the first half of the 20th century. At the time, cancer was more prevalent in Germany than in almost any other nation. According to the Stanford historian Robert Proctor, by the 1920s Germany’s escalating cancer rates had become a “major scandal.” A number of top Nazis, including Hitler, are believed to have harbored a particular dread of the disease; Hitler and Joseph Goebbels took the time to discuss new advances in cancer research in the hours leading up to the Nazi invasion of the Soviet Union. Whether Hitler was personally aware of Warburg’s research is unknown, but one of Warburg’s former colleagues wrote that several sources told him that “Hitler’s entourage” became convinced that “Warburg was the only scientist who offered a serious hope of producing a cure for cancer one day.” Although many Jewish scientists fled Germany during the 1930s, Warburg chose to remain. According to his biographer, the Nobel Prize-winning biochemist Hans Krebs, who worked in Warburg’s lab, “science was the dominant emotion” of Warburg’s adult life, “virtually subjugating all other emotions.” In Krebs’s telling, Warburg spent years building a small team of specially trained technicians who knew how to run his experiments, and he feared that his mission to defeat cancer would be set back significantly if he had to start over. But after the war, Warburg fired all the technicians, suspecting that they had reported his criticisms of the Third Reich to the Gestapo. Warburg’s reckless decision to stay in Nazi Germany most likely came down to his astonishing ego. (Upon learning he had won the Nobel Prize, Warburg’s response was, “It’s high time.”) “Modesty was not a virtue of Otto Warburg,” says George Klein, a 90-year-old cancer researcher at the Karolinska Institute in Sweden. As a young man, Klein was asked to send cancer cells to Warburg’s lab. A number of years later, Klein’s boss approached Warburg for a recommendation on Klein’s behalf. “George Klein has made a very important contribution to cancer research,” Warburg wrote. “He has sent me the cells with which I have solved the cancer problem.” Klein also recalls the lecture Warburg gave in Stockholm in 1950 at the 50th anniversary of the Nobel Prize. Warburg drew four diagrams on a blackboard explaining the Warburg effect, and then told the members of the audience that they represented all that they needed to know about the biochemistry of cancer. Source: http://www.nytimes.com/2016/05/15/magazine/warburg-effect-an-old-idea-revived-starve-cancer-to-death.html?_r=0 Low fat diets and exercise are pointless for those wanting to lose weight and obese people should simply eat less, a former shadow health minister told the House of Lords yesterday. Lord McColl, emeritus professor of surgery at Guys Hospital in London, warned that current health advice to avoid fat was ‘false and misleading’ and was fuelling the obesity epidemic.
Speaking at a House of Lords debate, the former surgeon warned that exercising was useless against the huge levels of calories from carbohydrates and sugars that people are now consuming. He warned that the obesity epidemic was as bad for public health as the 1919 flu epidemic. “In the UK the Department of Health and Nice (National Institute for Health and Care Excellence) maintains for many years that the obesity epidemic was due to lack of exercise,” he told peers. “It’s a pity that the 500 people employed by Nice didn’t think to go into the gymnasium get on a machine and exercise to see how few calories you actually burn off. One can pedal away on one of those machines for half an hour and only two or three hundred calories are burned up. One has to run miles to take a pound of fat off. “The whole subject has been bedevilled by all sorts of theories about the course of the obesity; genetics, epigenetic, psychological disturbances. None of them is the cause of the obesity epidemic. One fact remains. It is impossible to be obese unless one is eating too many calories.” In May the National Obesity Forum and the Public Health Collaboration called for a major overhaul of dietary guidelines saying 30 years of urging people to adopt low-fat diets was having ‘disastrous health consequences.’ Their report claimed the low-fat and low-cholesterol message, which has been official policy in the UK since 1983, was based on “flawed science” and had resulted in an increased consumption of junk food and carbohydrates. Lord McColl said eating fat was important because it kept people feeling fuller for longer, and advised overweight people to start adding fat into their diet. “Fat enters the small intestine and greatly delays the emptying of the stomach,” he told peers. “As the stomach emptying is delayed it gives the feeling that one has had enough to eat. Later when the fat has been absorbed the stomach then starts to empty again, It’s a beautifully balance mechanism which tends to prevent us from eating too much and prevents us from getting obese.” Researchers at Imperial College recently found that Britons are on course to be the fattest in Europe within a decade, with almost four in 10 people predicted to be dangerously overweight by 2025. Earlier this week, Sir Simon Stevens the chief executive of the NHS said the obesity crisis was now costing more than the police and fire brigade combined. “Obesity and its related illness is costing the country a fortune and it is not sustainable,” said Baroness Jenkin who called the debate in the Lords. “If we don’t wake up to the extent of this crisis the NHS could end up bankrupt. Already enormous amounts of money are spent on disease which are entirely preventable “The current dietary advice is confusing. The ‘Eat Well guide recommends potatoes, rice, pasta and other starchy carbs. Are we so sure that is good advice? We feed starchy crops to fatten animals so why would they not have the same effect on us?” Health minister Baroness Chisholm said: “There is no point going to an exercise class or a gym then going around the corner for a fizzy drink a donut. It is this sort of culture that needs to change. “Tackling obesity is an important issue. Obesity is a complex issue to which there is no single solution. “I would like to underline that Public Health England bases it dietary guidelines on comprehensive reviews. They consultant with academics, health charities and public health professionals.” Key conclusions | National Obesity Forum report Eating fat does not make you fat Evidence from multiple trials reveals that a higher-fat, lower carbohydrate diet is superior to a low-fat diet for weight loss and cardiovascular risk reduction Stop counting calories Calories from different foods have different metabolic effects on the body, so the cumulative calorie count is meaningless You cannot outrun a bad diet Obesity is a hormonal disorder leading to abnormal energy partitioning, which cannot be solely fixed by increasing exercise Saturated fat does not cause heart disease and full-fat dairy is likely to be protective New meta-analysis of the evidence available forty years ago does not support dietary fat restrictions Avoid at all costs: “processed foods labelled “low fat”, “lite”, “low cholesterol” or “proven to lower cholesterol” No single piece of evidence exists that demonstrates reducing dietary saturated fat reduces cardiovascular events and death Snacking will make you fat The increase in meal frequency plays an equal if not larger role in obesity and has largely been ignored. Source: http://www.telegraph.co.uk/science/2016/06/09/low-fat-diets-and-exercise-are-pointless-for-losing-weight-warns/ Chronic obstructive pulmonary disease or COPD is a lung condition caused by the body’s chronic inflammatory response to inhaled gases and particles. Bacterial infections may also contribute. Accumulated T lymphocytes attract inflammatory white blood cells that release proteases that breakdown of the connective tissue of the lungs. High concentrations of free radicals in tobacco and the chemicals released by inflammatory immune cells damage the cells lining small and large bronchial tubes leading to cell death and scaring or hyper secretion of mucus, hence chronic coughing. Usually, one pathology or the other predominates creating primarily emphysema or chronic bronchitis. Once the process gets started it’s difficult to stop even after quitting smoking.
Cannabidiol from organic hemp could stop this process by several mechanisms. First, CBD suppresses the T cells involved and prevents them from recruiting immune cells that damage the lung. Second, it blocks the inflammatory substances these cells secrete, like Tumor Necrosis Factor and Interleukin-6. Third, it inhibits bronchial tube constriction improving airflow. Fourth, it blocks acute lung injury to prevent the initial inflammatory response using adenosine cellular receptors. And Fifth, CBD increases lung function by decreasing airway resistance so exhaling is much easier. “CBD administered therapeutically, i.e. during an ongoing inflammatory process, has a potent anti-inflammatory effect and also improves the lung function. Case Study: 70 yo retired psychiatrist refinishing his sailboat mixed a stripping and cleaning chemicals that created chlorine gas in the confined space of his galley. He had immediate coughing and shortness of breath, was admitted per ambulance with oxygen support. He immediately started CBD by e-cigarette vaporization. His oxygenation was stable and he was discharged the next day. Cough and chest tightness resolved over the next 3 days with no residual impairment. In this case CBD appears to have halted a potentially serious lung injury and prevented the inflammation that could have lead to extended or chronic disease. Immunopharmacol Immunotoxicol. 2015 Feb;37(1):35-41. Pulm Pharmacol Ther. 2013 Jun;26(3):373-9 Eur J Pharmacol. 2012 Mar 5;678(1-3):78-85. CBD blocks narcotic addiction but now I am talking about alcohol, cocaine, heroin, and meth. CBD inhibits CB1 activation (Thomas, 2007) in the cell, brain and peripheral nerves. The result, from both theory and clinical experience, is the reduction of drug tolerance, addictive behavior and withdrawal. This means less drugs are needed to a...chieve the same benefits, the elimination of the addictive cravings and, very importantly, withdrawal prevention. I also want to add nicotine and benzodiazepines to the list of what I have seen clinically.
"Studies with drugs of abuse suggested that cannabinoid receptors are involved in the regulation of the central reward system. Accordingly, inactivation of cannabinoid CB1 receptors attenuates the rewarding effects of cannabinoids (Ledent et al, 1999), opiates (Ledent et al, 1999; Martin et al, 2000; Cossu et al, 2001), and cocaine (Chaperon et al, 1998), whereas stimulation of these receptors elicits relapse not only to cannabinoid consumption but also to cocaine, heroin, alcohol, and methamphetamine (Fattore et al, 2007; Higuera-Matas et al, 2008)." (De Chiara, Neuropsychopharmacology, 2010). http://goo.gl/J6T3mk We don't usually think about it but sugar evokes some of the same addictive properties as the worst addictive drugs..."Furthermore, the endocannabinoid system has a key role in the rewarding properties of palatable foods, and cannabinoid CB1 receptor blockade decreases motivation for sweet foods, whereas activation of these receptors increases it." Blair comments: This fact about the attenuation of all addictive compulsions with CB1 inhibition by CBD could lead to the most substantial public health improvement of the century. Study: Voluntary Exercise and Sucrose Consumption Enhance Cannabinoid CB1 Receptor Sensitivity in the Striatum http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055381/ |