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You don’t even have to eat more calories, eating the same amount of calories, but simply eating more fat, changed muscle function. Processed food manufacturers are in the business of making and therefore selling their food.
Foods that contain higher levels of salt, sugar, fat are the most likely to alter brain chemistry and cause people to overeat.
Swedish researchers tracked the increase of processed (116%) and ultra processed foods (142% increase) from 1960-2000. And the last study I read recently that I found fascinating and related is that high fat diets change your behaviour, and you probably already guessed it, not in a good way. High fat diets cause a number of problems, heart attacks and strokes are the most common, but now science has found that high fat diets can cause depression and other psychiatric problems. Visit the Start Here and Primal Blueprint 101 pages to learn more about the Primal lifestyle. Subscribe to my weekly newsletter to receive an eBook called Primal Blueprint Fitness and more - all for free.
Basically, the researchers fed a bunch of mice a high-fat diet designed to make them obese, which consequently raised the levels of free fatty acids (FFAs) in their blood.
In order to gauge your blood sugar and decide how much insulin to secrete, the beta cells in your pancreas have little glucose-sensors hanging out on their surface. Although this paper doesn’t give us a detailed description of what the mice were eating, it does reference the product numbers for their formula diets – so we can sleuth out the scoop straight from the manufacturer. Indeed, even if you believe high-fat diets can be healthy, it’s hard to find any redeeming qualities in this one.
But that doesn’t mean gene expression always works the same, or that the causes and progression of disease are identical across species.
I always take it with a grain of salt when the press demonizes high fat and high protein diets. Denise – you are a HUGE, MASSIVE part of the primal, paleo, ancestral, wapf, real food movement.
I would hope that after anyone in the world looks at what the mice were fed, they would dismiss the study. Not only is the calorie theory under attack, but evidence is also emerging to show that lowering fat might not cut heart-disease risk after all.A major study published in the authoritative New England Journal of Medicine compared the clinical benefits of a conventional low-fat diet with two types of Mediterranean diet, which are naturally considerably higher in fat. At the same time, as glucoseA  from carbs is turned into fat for storage in the body, fatty acids are also produced.It is this combination of fatty acids and low HDL, not saturated fat, that 'clogs your arteries,' says Dr Malhotra.
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Low fat, low salt, low carb, low sugar and low Glycemic Index (GI) food labels in metallic button. All plans come as a Standard license, and can be upgraded to an Enhanced license at any time. Going on a traditional cutting diet is going to do more harm than good at this point in your training. A way that will allow you to lose fat while building muscle at the SAME TIME so that you don’t have to worry about gaining a bunch of fat while gaining mountains of man muscle.
I’ll get into this special nutritional method in a minute but first I need to explain the major flaw in the old school cutting diet because I need you to completely understand why you MUST avoid it.
We as Skinny Fat guys typically don’t have a lot of muscle to work with when we’re starting out. Before I get into that I need to address another type of diet that is gaining in popularity right now that I whole heartily believe is the wrong way to go. You can go check out my program where I have this all broken down for you with diet plans for your specific weight.
So if you weight 170 pounds all you have to do is open the diet plan for 170 pound guys and you’re good to go. Slideshare uses cookies to improve functionality and performance, and to provide you with relevant advertising. Clipping is a handy way to collect and organize the most important slides from a presentation. School of Anatomy and Human Biology, the University of Western Australia, Perth, Australia.
School of Anatomy and Human Biology, the University of Western Australia, Perth, Australia.. The absence of functional dystrophin protein in patients with Duchenne muscular dystrophy (DMD) and dystrophic mdx mice leads to fragile myofibre membranes and cycles of myofibre necrosis and regeneration. This research is funded by the Australian National Health and Medical Research Council (MG) and Australian Postgraduate Award Scholarships (HR-C). Duchene muscular dystrophy (DMD) is characterised by progressive muscle weakness and wasting resulting from a lack of functional dystrophin that promotes increased myofibre membrane fragility, repeated cycles of myofibre necrosis and regeneration, and the eventual replacement of skeletal muscle by fatty and fibrous connective tissue. Dietary interventions in the form of various amino acids (with different biochemical effects) or other nutritional supplements have shown variable beneficial effects in both mdx mice and DMD patients [Reviewed in [7] [8] [32] [33] [34] .
A comparison of sedentary mice on a control diet, high fat diet or high protein diet between 8-24 weeks of age and 24-40 weeks of age.
Gastrocnemius muscle weight adjusted for bodyweight was significantly (P=0.045) heavier in mdx mice fed a control diet compared to C57 at 40 weeks of age (Figure 2C). A comparison of sedentary mice on a control diet with mice on either a high fat or high protein diet. Blood serum CK levels are always lower (approximately 10-fold) in C57 mice compared to mdx mice [18] [54] [55] and were not measured for C57 mice in this study. Data for dietary consumption between 8-12 weeks of age is shown for both sedentary and voluntarily exercise mdx mice on either a control diet, high fat diet or a high protein diet.
Voluntary wheel exercise for 4 weeks caused no change in the body weight of 12-week-old mdx mice, and neither did consumption of a high protein or high fat diet (Figure 8A). Exercise was completely voluntary and distance run is an indirect indicator of muscle function and exercise capacity. Voluntary exercise increased (P=0.02) myofibre necrosis (% CSA) in the quadriceps muscle from 12-week-old mdx mice approximately twofold, relative to the amount present in sedentary mice. To our knowledge, the response of adult mdx mice to a high fat diet has not been described previously.
Dystrophic mdx mice were significantly heavier than control C57 mice at both 8 and 24 weeks of age (Figure 2A), primarily due to a well described increase in muscle mass [52] [55] [59] [60] [61] [62] [63] . The muscular body composition of mdx mice (<40 weeks) is in stark contrast to DMD patients who can move between the spectra of over-nutrition (and obesity) to under-nutrition within their shortened lifespan, and who lose muscle mass at a rate of 4% per year as adults [7] [34] [64]. The 8 – 24-week-old mdx mice consumed similar amounts of food and energy compared to age-matched C57 mice across the 3 diets (Figure 1A-C). In contrast to mdx mice, after consumption of a high fat diet (for 16 weeks) C57 male mice at both 24 and 40 weeks had significantly greater body weights most likely due to a gain in epididymal fat pad weight (and presumably other body fat) (Figure 2A, B) with significant accumulation of adipocytes in the quadriceps muscle of 40-week-old mice (Figure 4B).
The lack of any benefits with the high protein diet contrasts with studies in mdx mice that show mildly reduced dystropathology after dietary supplementation of creatine, taurine and glutamine (both alone and in combination with prednisolone) [8] [25] [37] [38] [40] . A prolonged positive imbalance between energy intake and expenditure resulting in obesity, is associated with chronic inflammation and may be a potential mechanism by which obesity leads to insulin resistance (in both humans and mice) [Reviewed in [44] [46] [69]. Due to the multiple systemic effects that the 3 PPARs and PGC-1? have on whole body metabolism (e.g. In order to further examine the potential benefits of a high fat or high protein diet on dystrophic muscle, 8 – 12-week-old mdx mice were voluntarily exercised to exacerbate the dystropathology [1] [49] [50] [54] .
Despite a high fat diet reducing myofibre necrosis in sedentary 24-week-old mdx mice (Figure 4), this diet had no significant benefit on myofibre necrosis or serum CK levels in voluntarily exercised mdx mice. This research clearly identifies an ‘altered’ response to a high fat diet in dystrophic muscles of mdx mice compared to C57 controls. The authors thank Mr Greg Cozens (School of Anatomy & Human Biology, UWA) for excellent technical assistance, Dr Andrew Hoey (University of Southern Queensland) for consultation regarding the preliminary studies and Mr Warren Potts (Specialty Feeds, WA) for design and manufacture of the three semi-purified diets. Protein comes from animals and plants and provides us with everything we need to build and maintain our muscles. Protein is found in fish, meat, poultry, dairy, eggs and tofu, as well as beans, vegetables and fruit. Incomplete proteins, however, are not sufficient protein sources by themselves.  As a result, you need to eat several incomplete proteins to get all of the amino acids your body needs. To ensure we are comparing apples to apples, so to speak, we are going to focus on complete proteins. I am happy for reading this page because i learnt much from it and i have been looking for ways to reduce my weight but i thank you for leting me know some lesson about the food we eat. We’ve lived through decades of fat demonetization, and recently carbs have taken center stage as the macronutrient of Lucipher. As we know, neither one of these macronutrients are bad in themselves, despite fashionable trends. Xand (left) and Chris (right) Van Tulleken test to see which works best for them: a no-carb diet or a high-carb diet. The BBC documentary Sugar v Fat, was presented by two identical twins, doctors Chris and Xand Van Tulleken, who both went on opposite diets for a month.
Professor Paul Kenny, who makes a mark in the second half of the show, has tested different ratios of fat to sugar on rats, to see which they find most palatable. The little guys lost all interest in healthy food, and would constantly graze their hunk of junk all day long. Companies have been combining fat and sugar ever since the birth of the industrial food industry to encourage people, like the lab rats, to graze on their products as much as possible, and to lose interest in other food. The closing message is that processed foods often combine carbs and fat into a lethally addictive combination, to stay away!
While the final point is to cut down on foods that combine carbs and fat, the rest of the show tries to convince us that limiting either one is dangerous.
The high-fat twin, Dr Xand, stuck to a 0% carb diet that had him “remove all fruit and veg” because “they have carbs”, while the high-carb twin, Chris, kept 2% of his calorie intake from fats because “you need some fat to survive”. If they wanted to be scientific, keeping 2% of his calorie intake from carbs would have made the playing field much more even. If you want to lose weight and reduce inflammation, you can do so by cutting carbs, but maintain at least 30g a day, and get them from vegetables. The insulin hypothesis never did undercut the idea that you have to store more energy than you use in order to gain weight. What it does undercut is the woefully ineffective weight-loss method of forcing yourself to eat less and exercise more, without paying any attention to the quality of your food.
You can lose weight on a high-carb diet by restricting calories, but it’s torturously difficult. You can see this effect on the high-carb twin, who “never felt full, so was constantly snacking”.
Only a few of the foods pictured here were allowed to Xand on his highly restrictive no-plant diet. This means companies that produce, for example, statins, payed money to the man who wrote the text-book which taught your doctor that if you have high cholesterol, he should put you on a course of statins. Unfortunately, the same financial incentive doesn’t exist for the advice of eating an optimal diet.
This may help explain why nutritional therapy is so poorly taught, despite how safe and effective it is in treating chronic disease.
First we’ll start with the “amazing” results that would seem commonplace to anyone in the low-carb or paleo diet space. The scene goes on to show them having their fasting glucose and insulin sensitivity tested.
This essentially means that when you drink a litre of Gatorade, you won’t feel the effects of the drink as much if your body can churn out a ton of insulin. I’m afraid there is some evidence that saturated fat (only) can worsen insulin sensitivity. Richard seems to be listening only to the evidence that supports the tired old idea that fat makes you sick. Secondly, why is it a bad thing that Xand didn’t flood his blood with so much insulin when he gave himself the big spike in sugar? Richard’s idea that all this meant Xand would one day stop producing any insulin was pure conjecture. We also can’t know if these levels would have kept rising if he had kept it up for another month. The implication that he was on a freight-train to full blown diabetes was, again, reactive conjecture. Possible, but not scientific to say it was definitely happening, let alone decide what caused it. It’s always inspiring to see people taking action and experimenting with different lifestyles to see how it affects them. The experiences of these two identical twins does not directly translate into the experiences of you and me. If you’d rather base your life decisions on scientific analysis, (rather than on vague implications, ruthlessly edited and presented on a background of manipulative music), then take a look at analyses like this one, which looks at 23 gold-standard scientific studies, all comparing the results of low-fat vs low-carb diets.
Be inspired to run your own self-experiments, and remember that the types of carbs and fats make a huge difference. Get Updates (It’s Free)Learn how to burn fat and retrain your eating habits with the Modern Life Nutrition newsletter.
A high fat diet plan, when combined with carbohydrates, can delay weight loss, while a high fat dietary composition coupled with a low level of carbohydrates (the most common type) will burn muscle, slow metabolism, and actually make the likelihood of long term fat gain quite high.
To lose weight efficiently and consistently, a proper blend of protein, carbohydrate and fat is necessary, and a high fat and low carbohydrate meal composition will not produce desired results. No matter what I tried, I just couldn't lose the excess weight I had gained during my 3 pregnancies.
I am now pursuing a modeling career and I thank you for helping me by writing this program.
I lost 40 pounds, and the best part of the program for me is that Francesco gives free lifetime personal training via email. I would like to thank you again for your work, and I am grateful to have the opportunity to learn from you. I’m very happy to say that I did this without costly supplements that can be harmful to your health.
It is awesome to see how so many people are amazed at the results that I have achieved.  Just look at the definition in my abs and obliques!
I would not of believed it at the start that your Fat Vanish program could be so potent and change my body so dramatically. There are plenty of times you might eat high fat foods, not only on holidays and vacations, and it only takes 5 days to change your metabolism.
Since 1980, when 857 million were classified as obese or overweight to 2013 when that number rose to 2 billion, 3-4 million people die yearly from related complications. Another study that just came out proves that the more highly processed foods are linked to addictive eating. Instead of being satisfied, eating these salt, fat, sugar combos are more likely to cause you to want more.
Processed foods have high calorie density but low nutritional density and the increased intake mirrors the obesity rates in Sweden. Processed food did with all the variations on how we can eat it, then we couldn’t stop.
If you want to lose weight, gain muscle, increase energy levels or just generally look and feel healthier you've come to the right place. There you'll find books, food, and the best supplements on the planet to help you take control of your health for life.

Although we’ve known for a while that FFAs interfere with glucose metabolism, this study uncovered a new piece of the obesity-diabetes puzzle. Those sensors are maintained by an enzyme called GnT-4a glycosyltransferase (can we call it George for short?). To clarify the pathway in non-mice, the researchers grabbed some cell samples from humans and cultured them with palmitic acid, a fat sometimes used to simulate the effect of free fatty acids. Are high-fat diets going to make us obese, fill our blood with free fatty acids, and push us to the brink of diabetes? Along with being easy to breed, they’re uber-susceptible to obesity, high blood sugar, insulin resistance, leptin resistance, and all that other fun stuff plaguing modern humans.
For starters, the primary fat is a hydrogenated oil, which doesn’t belong in the body of any living organism, whether two-legged or four. Although most mice turn into metabolically deranged messes when they eat too much fat (which makes sense, considering their natural diet is mostly grains), not all of them succumb to the same fate. As this paper explains, there’s literally no standard for what “high fat” means, and rodent researchers have thrown everything from 20%-fat diets to 60%-fat diets under the same “high fat” umbrella. As we might expect, researchers found that mice eating a moderately high-fat diet became obese, leptin resistant, and insulin resistant – but when they dropped the sugar and increased fat to around 78% of calories, the mice “lost all excess body weight, improved glucose tolerance, and increased energy expenditure” without even reducing calorie intake.
Does this study – or rodent research in general – have much relevance for those of us who lack tails, fuzzy ears, and adorable pink noses?
Even when high-fat diets catapult mice towards diabetes, for instance, their markers for disease don’t always resemble ours. We have enough high-fat, low-carb research at this point to know that such a diet won’t cause an unstoppable snowball towards obesity in humans like it does in some mice.
Either the authors of those 2 articles, that have vegans throwing parties, did not read what the mice ate or they dismissed it completely because they are vegans themselves. Have 50 of them go Primal, the other 50 do something conventional like Weight Watchers or Jenny Craig, with all doing whatever exercise they want, and see what happens. I tried Weight Watchers several times; not only was it the biggest drag, but my fat barely budged, whereas when I did Atkins I had rapid results that endured.
By the way, Denise’s dad has just lost 10 lbs in one week following the Primal Blueprint!
Indeed, Professor David Lawrence, an expert in nutrition and obesity data analysis, said recently in the journal BMC Medicine thatA  the idea is based 'on an outdated understanding of the science'.The sceptics argue that calories from different sources have different effects on the body, with calories from carbohydrates more likely to encourage weight gain.
For three weeks he got these calories from a low-fat, high-carb diet; for another three, he ate more fat and cut right back on carbs. Recent research supports the idea that warning about saturated fat in the diet has probably been a mistake. Everyone who signs up gets full access to our entire library, including our curated collections.
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It is proposed that both DMD patients and mdx mice have an altered metabolism and impaired energy status and that nutritional supplementation may reduce the severity of dystropathology.
The specific mechanism(s) responsible for myofibre necrosis are still unclear, although there are strong associations with excessive inflammation, increased intracellular calcium levels, elevated oxidative stress, and metabolic abnormalities [1] [2] [3] [4] [5] [6] [7] [8] . Studies in both DMD patients and mdx mice indicate that dystrophin defects may also lead to altered skeletal muscle metabolism and an impaired energy status. Recently completed clinical trials have examined the safety and role of specific amino acid supplementation (creatine and glutamine) in DMD patients and demonstrated some beneficial effects [35] [36] .
Diet specifications for the 3 semi-pure diets used in this study: control (AIN93g), high protein (SF00-252) and high fat (SF06-40).
The low level of muscle damage in dystrophic adult mdx mice can be exacerbated by voluntary exercise [18] . The quadriceps muscles were dissected and immediately fixed in 4% paraformaldehyde (Sigma P6148) for 48 hours. Non-overlapping tiled images of transverse muscle sections provided a picture of the entire muscle cross section. While under terminal anaesthesia blood from the mdx mice was collected via cardiac puncture. Consumption of the high fat diet induced many changes in the body composition of both C57 and mdx mice, whereas the high protein diet did not.
There was no significant difference in the body weights of 40-week-old C57 mice and mdx mice on the control diet (Figure 2A); nor did the high protein diet have any significant effect of the body weight of either strain of mice (Figure 2A). The high protein diet had no impact on the epididymal fat pad weight in either strain of the older mice.
There was no difference in the average myofibre CSA in the tibialis anterior (TA) muscle from 12-week-old C57 and mdx mice on the control diet (Figure 3).
Myofibre necrosis (% CSA) was significantly (P=0.04) decreased in the quadriceps muscle of 24-week-old mdx mice fed the high fat diet and was approximately half the amount present in mice fed, the control diet (Figure 4A). There was no change in the level of myofibre necrosis in the quadriceps muscle between 24 and 40 week old mdx mice (Figure 4A) and no effect of either the high protein or high fat diet on myofibre necrosis in 40-week-old mdx mice (Figure 4A). There were no significant changes in inflammatory cytokine mRNA levels with age in either strain of mice fed the control diet. Mdx mice were voluntarily exercised for 4 weeks to increase the low level of dystropathology in skeletal muscles [1] [50] [ 54]. Mdx mice fed the high fat diet ran approximately 50% further (P=0.003) during 4 weeks of exercise (compared to mdx mice on the control diet (Figure 9A). The high fat diet for 4 weeks had no effect on myofibre necrosis in either voluntarily exercised or sedentary mdx mice. In contrast, 40-week-old mdx mice were the same weight as C57 mice; this equalising in bodyweight occurred at approximately 32 weeks of age (data not shown) and was most likely due to an increase in body fat in C57 mice (Figure 2B). It is important to consider that the striking loss of muscle mass in DMD patients occurs during the growth phase of the boys (approximately 20 years). Yet, there was a large difference in the way the two strains of mice responded to the high fat diet.
Consumption of either diet for 16 weeks did not reduce levels of serum CK (an indicator of myofibre leakiness), even though the high fat diet reduced by approximately 2.5-fold myofibre necrosis in the quadriceps muscle of 24-week-old mdx mice. Taurine is not a substrate for protein synthesis, but may improve dystropathology via regulation of calcium homeostasis [67] . Although the 12-week-old mdx mice were very lean, there was a further reduction in epididymal fat pad weight after 4 weeks of voluntary exercise (Figure 8B).
Energy intake was significantly increased in voluntarily exercised mdx on the high fat diet compared to mdx mice on the control diet (Figure 7B). This response was pronounced in younger mdx mice<24 weeks old, but diminished with age (by 40 weeks).
Research funding from the Australian National Health and Medical Research Council (MG) and Australian Postgraduate Award Scholarships (HR-C) are gratefully acknowledged.
Reduced muscle necrosis and long-term benefits in dystrophic mdx mice after cV1q (blockade of TNF) treatment. The chart below does not include all foods that contain complete proteins, but it provides a good cross-section of popular foods.
The same price as other pastas, but a low glycemic index, far less calories and carbs and tastes like REAL pasta!
That way you’ll also be benefiting from the vitamins and minerals that are difficult to obtain from animal sources. It simply states that refined carbohydrates encourage your body to store energy rather than use it, which makes you hungry and lures you into eating more. It’s an improvement for your pancreas to readily flood the blood with huge amounts of insulin? Since this was so far from a controlled trial, we can’t know that the fat in his diet was causing it through a reduction of insulin sensitivity.
Drop your questions and insights into the comments below, or enter your email address in the box below to get access to me directly. I lost over 50 lbs of fat, and am teaching men and women around the world how to lose weight and burn fat naturally through my proven Fat Vanish weight loss diet plan. But with Fat Vanish, I lost 49 pounds in 3 months, and I have never felt sexier and healthier. The results I have experienced really have proven to me the total effectiveness of the MuscleNOW product.  IT IS FANTASTIC! The program is flawless, your money back gaurantee is safe, anyone who works the plan will get the results.
Your muscles make up about 30% of your weight and are responsible for breaking down or storing glucose for energy. Muscle is critical for normal glucose metabolism and can have dramatic consequences to your health if normal metabolism is changed. The doctor and lawyer David Kessler, author of The End of Overeating, says the food industry manipulates our brain’s neurological response and designs foods to make us eat more then we should. Your mom left four voicemails ordering you to throw away your bacon now (and clean your room while you’re at it).
This is a classic example of the media spinning an article to help it grab attention, because most people wouldn’t give a flying Fudgsicle if they knew what it was really about. As this study discovered, high levels of FFAs interfere with two of the proteins necessary for producing GnT-4a (er, George), leaving beta cells unable to figure out how much glucose is in your blood.
Lo and behold, the fat interfered with the same two proteins that got goofed up in obese, FFA-ridden mice. They’re also genetically predisposed to getting type 2 diabetes, making them particularly useful for the study at hand. As far as obesity goes, rodents have dramatically different responses to the types of fat they eat—with rats, for instance, getting tubby from lard but slimming down with marine oils. Black sixes are one of the unlucky types that get rapidly obese on high-fat diets, but some other strains remain lean on the same cuisine and are far more resistant to diabetes. Unlike metabolically damaged humans, who tend to have rock-bottom HDL cholesterol and rising triglycerides, some mice experience higher HDL and unchanged (or reduced!) triglycerides when eating the diets that make them diseased (PDF). Come talk to me when a study is done with 100% real, whole, paleo approved food vs a standard american diet that fulfills the dietary government guidelines. Based on a review of 16,000 studies, it said the best sorts of food for losing weight were the likes of olive oil, double cream and bacon. He did exactly the same, moderate exercise regimen each time.Now, according to the conventional wisdom, the weight gain would be the same on both regimens. Add to that the increase in his waist measurement, and he was looking a lot less healthy than he had been.'What's more, a level of inflammation in his liver had doubled, which is also linked with diabetes and heart disease. If at any time you're unsatisfied with your experience with us, you can cancel your subscription. Corticosteroids remain the standard pharmacological treatment [9] [10] [11] [12] although promising approaches to replace the defective dystrophin gene have been extensively investigated over the last 10 years [13] [14] [15] [16] [17] .
Repeated cycles of myofibre necrosis and regeneration, increased demand on the sarcoplasmic reticulum to regulate intracellular calcium, defective mitochondrial function, increases in both protein synthesis and protein degradation rates, altered oxidative stress and disruption in nNOS signalling may all contribute to an altered metabolic state [4] [22] [23] [24] [25] [26] [27] [28] [29] [30] .
The dystropathology of skeletal muscles was not examined in this study, but these results led us to propose that due to their altered energy flux, a high fat diet may reduce the extent of dystropathology and may be metabolically beneficial to mdx mice. Group 1) sedentary C57 and mdx mice fed a custom diet from 8-24 weeks of age, Group 2) sedentary C57 and mdx mice fed a custom diet from 24-40 weeks of age and Group 3) voluntarily exercised mdx mice fed a custom diet from 8-12 weeks of age.
Mdx mice were caged individually with free access to a voluntary running wheel for 4 weeks (from 8 to 12 weeks of age). Total body weight, epididymal fat pad weight, and gastocnemius muscle weight were recorded immediately.
Muscles were then placed into 70% ethanol, processed in a Shandon automatic tissue processor overnight, and finally paraffin embedded for sectioning. Therefore gene expression was quantified only in mice which consumed the control or high fat diet. All variables were analysed by ANOVAs (to account for diet, strain, age, and exercise) and Least Significant Difference (LSD) post-hoc tests.
The high protein diet had no significant impact on epididymal fat pat weights in either strain of mice; fat pads remained heavier in C57 mice compared to mdx mice. On the high fat diet, there was a slight increase (but not significant P=0.38) in body weight-adjusted epididymal fat pad weight of C57 mice (Figure 2B). Between 12 and 24 weeks of age, myofibres in the mdx TA continued to grow (hypertrophy) and were significantly larger on average than C57 myofibres at 24 weeks of age (P=0.02) (Figure 3).
The high protein diet had no effect on the adipocyte content of the quadriceps muscle in either strain of 40-week-old mice.
Increasing the extent of dystropathology allowed for further evaluation of the potential beneficial effects of a high protein or high fat diet in mdx mice. There was no difference in distance run by mdx mice fed the high protein diet compared to the control diet. The high protein diet had no effect on sedentary mice, but significantly (P=0.04) increased myofibre necrosis in exercised mdx mice) (Figure 9B).
The CK levels in mdx mice were not affected by a high protein or high fat diet (data not shown).
It is commonly accepted that obesity occurs when there is a chronic positive imbalance between energy intake and energy expenditure, and that long-term consumption of a high fat diet increases deposition of adipose tissue and eventually leads to obesity in both sedentary laboratory rodents and humans [Reviewed in [46] ]. The body weight of mdx mice did not increase between 24 and 40 weeks of age, nor was there a change in relative epididymal fat pad and gastrocnemius muscle weights (Figure 2A), supporting reports that there is a stabilisation of the dystrophic phenotype in adult mdx mice [18] [52] .
In contrast to the C57 mice, the mdx mice<24 weeks of age did not deposit significant body fat. It is possible that a high fat diet (and increased energy intake) assists mdx mice metabolically and thus helps them to maintain skeletal muscle structure and mass, or that increased lipid coming from the high fat diet stabilises fragile membrane lipids and prevents myofibre necrosis. These increases in gene expression were not seen in mdx mice (Figure 5A-C) which demonstrates, in addition to the lack of changes in body composition, the resistance of mdx mice (particularly<24 weeks) to a high fat diet. However, the precise consequence(s) in dystrophic skeletal muscle, to our knowledge, are not documented.
It appears that mdx mice were able to maintain body weight and muscle mass (Figure 8A, C) over 4 weeks of voluntary exercise by increasing food consumption and energy intake (Figure 7A, B). This may have enabled the mdx mice to run further (approximately 50%) without producing further muscle damage (e.g. Therefore, it is proposed that the increased capacity for exercise in dystrophic mdx mice fed a high fat diet may be modulated, in part, via up-regulation of the 3 PPARs and PGC-1?. The high fat diet appears to have enabled the mdx mice to better meet their energy needs, and reduced the severity of their dystropathology and increased their voluntary exercise ability.
I mix 1 cup cooked elbows with a single serve can of tuna, with a tablespoon of non-fat yogurt, a tablespoon of parm, sprinkle it with fresh parsley and fresh cracked pepper-a taste sensation in 10 minutes with like 30 grams of protien and just over 300 calories!! Any one of us could do the same experiment, only it would take us two months to get the results of both diets, rather than one. When that happens, those cells can’t release the right amount of insulin to keep your blood sugar in check. And perhaps most importantly, all it takes to send them into a downward spiral of disease is some extra dietary fat. And hydrogenation aside, some mice strains gain different amounts of weight when their high-fat diet consists of unsaturated fats rather than saturated fat.
Not only does this make the rodent literature hard to navigate, but it also gives an incomplete picture of the effect of diet on obesity – because something special happens when mice get a truly high-fat menu.
This points to some clear differences between how humans and mice experience diet-induced metabolic problems.
So even if weight gain (and the associated increase in free fatty acids) sets us down Diabetes Avenue, a high-fat diet isn’t necessarily the instigator in humans. So when it comes to studies like this one, white out the headline, read with an open but critical mind, and then invite Mother Dearest over for a bacon brunch.

Consumption of a high protein diet had minimal effects on the body composition or muscle morphology in both strains of mice. Clearly, studies to identify strategies that will mitigate the muscle damage and sustain efficient repair are warranted. In addition, creatine, taurine and glutamine treatments have shown various benefits in treadmill-exercised adult mdx mice [37] [38] .
All animal experiments were conducted in strict accordance with the guidelines of the National Health and Medical Research Council Code of practice for the care and use of animals for scientific purposes (2004), and the Animal Welfare act of Western Australia (2002), and were approved by the Animal Ethics committee at the University of Western Australia. All mice were fed a standard (cereal-based) mouse chow (meat free, 5% fat, 19% protein) prior to the study. Exercise data were collected via a small magnet attached to the mouse wheel, and a sensor from a bicycle pedometer attached to the back of the cage.
Blood serum was collected via cardiac puncture, the gastrocnemius muscle was snap frozen in liquid nitrogen for gene expression analysis and the quadriceps and tibialis anterior (TA) muscles were collected for histology. Blood serum creatine kinase (CK) analysis was completed at the Murdoch Veterinary Hospital, Murdoch, WA.
RNA was extracted from snap frozen gastrocnemius muscles, DNAse treated, reverse transcribed into cDNA and purified. This difference in body weight was maintained throughout the study until 24 weeks of age for mice on the control and high protein diet (Figure 2A). After consuming the high fat diet, the epididymal fat pad weight adjusted for body weight was significantly (P=0.015) higher in C57 mice compared to C57 mice fed the control diet (Figure 2B) and, at sacrifice, large amounts of adipose tissue were conspicuous around the sternum, kidneys and hip joints. Neither the high protein nor high fat diet resulted in any differences in standardised or absolute gastrocnemius muscle weight in either strain of mice. Consumption of the high fat diet also significantly (P=0.04) increased the body weight of the older mdx mice (Figure 2A). There was no change in gastrocnemius muscle weight adjusted to bodyweight in mdx mice between 24 and 40 weeks of age. Dystrophic myofibres do not continue to hypertrophy and average myofibre CSA in 40-week-old mdx mice was significantly reduced (P=0.025) compared to 24-week-old mice and not different from the average mdx myofibre CSA at 12 weeks of age.
No significant change in standardised or absolute gastrocnemius muscle weight was seen after voluntary exercise or diet change (Figure 8C). Obesity is associated with numerous changes in cell signalling that are believed to underlie much of the morbidity associated with the condition [Reviewed in [46] [57] [58] ]. Both 24 and 40-week-old mdx were very lean, with significantly smaller epididymal fat pads, larger gastrocnemius muscles and larger myofibres CSA compared to C57 mice (Figures 2B, 2C, 3). We propose that the reduced myofibre size in 40-week-old mdx mice is probably due to myofibre splitting or branching. Amino acid supplementation is already widely used amongst DMD patients despite there being no conclusive supporting evidence in the literature [7] [12] .
Inflammation plays a major role in myofibre necrosis and regeneration in skeletal muscle, thus the inflammatory state can be an indirect indicator of the extent of dystropathology [1] [42].The high fat diet significantly reduced PGC-1? gene expression in 24-week-old C57 mice but, apart from this, there were no other significant changes in PPAR expression caused by the high fat diet in either strain of mice.
She’s likely to get light headed pretty quickly, because her liver is not used to dealing with the toxins in the drink. Especially not a high-fat diet that’s based on real food instead of hydrogenated coconut oil. I was really surprised that the damaging changes had happened so quickly.' Did the fact that, as a personal trainer, Sam was obviously veryA  fit at the start of his trial makeA  a difference?
A combined nutritional therapy (creatine monohydrate, conjugated linoleic acid, ?-lipoic acid, and ?-hydroxy-?-methylbutyrate) administered, in addition to prednisolone, for 8 weeks increased muscle strength and reduced the extent of dystropathology in 12-week-old treadmill-exercised mdx mice [39] . The pedometer records single wheel revolutions, allowing total distance (km) run by an individual mouse to be determined, as per [1] [49] [50] . Histological analysis was carried out on whole cross sections of the quadriceps muscle (dystropathology and adipocyte content) and the frozen TA muscle (myofibre CSA). After consuming the high fat (HF) diet for 16 weeks, the final bodyweight of 24-week-old C57 mice was significantly greater (P=0.04) than for C57 mice on the control (C) diet. In contrast, 24-week-old mdx mice fed a high fat diet were very lean and had small epididymal fat pads, similar in weight to mdx mice fed the control or high protein diet (Figure 2B).
The largest increase in body weight (group average) was seen in C57 mice on the high fat diet.
There were no significant differences in adipocyte content of the quadriceps muscle in 24 week old C57 and mdx mice after consuming any of the 3 diets. The high fat diet also significantly increased adipocyte content between 24 and 40-week-old mdx mice (Figure 4B).
Expression of the three PPARs was unchanged in either strain by consumption of the high fat diet. PPAR alpha mRNA was approximately twofold lower (P=0.02) in the gastrocnemius muscle of 40-week-old mdx mice compared to C57 mice (Figure 5A). Shavlakadze et al (2010) reported no difference in myofibre CSA in the quadriceps muscle between 12 and 52 weeks due to significant myofibre splitting in 52-week-old mdx mice [52] . The older mdx mice (24-40 weeks) were susceptible to the negative effects of a high fat diet, showing significant increases in total body weight and standardised fat pad weight compared to those on the control diet (Figures 2A, B).
It is important to consider possible counteracting effects when combined interventions are administered. It has also been shown that several gene programmes linked to PGC-1? are dysregulated in dystrophic muscle (e.g.
A possible interpretation is that the high fat diet was able to better meet the increased energy needs of the mdx mice thereby enabling them to run further while also maintaining myofibre integrity. This study in mdx mice raises many interesting questions about possible differences in metabolism and energy demands between dystrophic and normal muscle. A new study tracking more than 157,000 US households for one year shows that highly processed foods make up more than 60% of the calories in the food we are buying.
Pilot trials were conducted prior to commencement of the study to ensure that all diets were palatable. In contrast, there was no difference in the bodyweight of 24-week-old mdx mice fed the high fat or control diet (Figure 2A).
In the abdominal cavity, the epididymal fat pads often of mdx mice could not be seen until the testes were pulled up into the abdominal cavity.
The average changes in body weight for C57 mice (% change of sample group) were 116% after control diet, 102% after high protein diet and 141% after high fat diet. The 40-week-old mdx mice were still very lean with no change in the body weight adjusted epididymal fat pad weight between 24 and 40 weeks of age for mdx mice fed a control diet (Figure 2B).
However, PGC-1? was reduced significantly (P=0.02) in 24-week-old C57 mice fed the high fat compared to the control diet.
The high fat diet caused no change in the mRNA levels of the 3 PPARs or PGC-1? in either strain of 40-week-old mice.
Since our study examined myofibre CSA at 24 weeks and identified significant myofibre hypertrophy in mdx mice at this age, it seems that myofibre splitting occurs sometime beyond 24 weeks, but before 40 weeks of age.
A high protein diet or supplementation with certain amino acids (such as leucine) can stimulate skeletal muscle protein synthesis in both young and adult animals, but there is a threshold of protein requirement for maximum growth and once reached, additional protein intake does not further stimulate protein synthesis in skeletal muscle [Reviewed in [66] . For example, our data from mdx mice on the high protein diet (which contains increased concentrations of the essential amino acids such as leucine and phenylalanine used in protein synthesis, but without an increase in metabolisable energy intake – Table 1) do not support such an intervention since elevated myofibre necrosis was observed in response to voluntarily wheel exercise. The extent to which this benefit of a high fat diet is due to an increased energy intake per se, or to specific benefits of increased dietary fat directly on dystrophic muscles is not yet clear: determining the precise mechanism responsible for these demonstrated benefits is an important future goal. The most important of these hormones, and the one that's crucial for weight loss, is insulin.
After all, Sam's high-fat diet has close parallels with the Atkins diet - a low-carb diet which has been linked with side-effects ranging from bad breath and constipation to more serious problems including a lack of bone-building calcium and kidney problems. In contrast, after consuming the high fat diet for 16 weeks the mdx mice (< 24 weeks) remained lean with minimal fat deposition and were resistant to changes in body composition. Throughout the study mice were caged in groups of 4-8 and group body weights were measured weekly, mice were not tracked individually for the duration of the study. Throughout the experiment the mice were monitored daily for food consumption and distance run. The TA muscles were collected, and embedded in tragacantch gum (Sigma Aldrich G1128) mounted on a small cork block, and quenched in isopentane cooled in liquid nitrogen. The largest gain in body weight (group average) between 8 and 24 weeks of age was seen in the C57 mice fed the high fat diet.
The average changes in body weight for mdx mice (% change of sample group) were 103% after control diet, 94% after high protein diet and 110% after high fat diet. The body composition of mdx mice changed between 12 and 24 weeks of age, with significant increases in body weight, absolute and standardised gastrocnemius muscle weight and individual myofibre CSA (Figures 2A, 3, 8A).
Therefore, it is possible that in well-nourished sedentary mice (with adequate protein intake), the high protein diet had no effect on muscle mass. Overall there seems to be an association with decreased PGC-1? expression having detrimental effects in both dystrophic and normal muscle. In addition, the effects of a high fat diet on dystrophic heart function and pathology needs to be addressed in mdx mice, before considering translation to the clinical situation. Group food intake was monitored twice weekly by subtracting from a pre-weighed amount, the food that remained in the food compartment on the cage lid, and food inside the cage that could be separated from the cage bedding.
The average changes in body weight for C57 mice (% change of sample group) were 130% after control diet, 140% after high protein diet and 159% after high fat diet. There was no effect of the high fat diet on the standardised gastrocnemius muscle weight in mdx mice. Additionally, the utilization of dietary protein for anabolic processes is dependent on the adequacy of energy intake. It is appreciated that in corticosteroid-treated inactive DMD patients, a high fat diet may contribute to obesity and thus impact on disease severity (especially since corticosteroid usage is known to contribute to obesity and Cushingoid symptoms).
A high-carb diet increases the amount of glucose in the bloodstream, which in turn means you produce more insulin.
That is to misunderstand how fat storage works.'Research has already shown that if you are eating a high-carb diet, and so have high levels of insulin, you are likely to have more fat in your blood than someone on a high- fat diet.
Furthermore,A  those eating low-carb these days are much more flexible about the amount of fat they get. TA sections were stained with Sirius red to distinguish myofibres (yellow) from collagenous myofibre membranes (red), and which allows for easy and accurate quantification of myofibre cross-sectional area (CSA).
The average changes in body weight for mdx mice (% change of sample group) were 130% after control diet, 132% after high protein diet and 137% after high fat diet.
If the energy requirements of the mdx mice were increased, and not met by a corresponding increase in intake, dietary amino acids would be preferentially oxidized for energy rather than used for protein synthesis. In addition, the impact of a high fat diet might be different in steroid-naive DMD boys and also influenced by growth and disease severity.
Research is still needed to sort out the best ratio of carbs to fat.NO CHANGE TO OFFICIAL ADVICE So will UK dietary experts soon be recommending a Swedish style U-turn in healthy eating advice? Additional, more mechanistically based research will be required to establish optimal dietary interventions to reduce the severity of dystropatholgy and maintain muscle function for potential application to DMD. Distinct areas of active myofibre necrosis and very early muscle regeneration (small myotubes) were not included in myofibre cross sectional area analysis. While it is possible that a beneficial response to high protein consumption might be seen in combination with resistance exercise, such demanding exercise is usually not recommended for dystrophic boys or animal models of DMD due to additional damage to dystrophic muscles. A low-carb diet means less insulin, making it easier to lose weight because less fat is then stored. Impaired mitochondrial oxidative phosphorylation in skeletal muscle of the dystrophin-deficient mdx mouse. MORE CALORIES,A  BUT SLIMMER WAIST Dramatic new evidence for this has come from a unique experiment conducted by a personal trainer from East London.
She says Sam gained weight 'more slowly on the high-fat diet - but if he had continued with them for longer, I suspect the two diets would have ended up producing the same amount of weight gain.
In fact, he says, it's too many carbs that are the problem.He argues that - as seen with Sam - a high-carb diet tends to lower the good HDL cholesterol that helps keep arteries clear. Dysregulated intracellular signaling and inflammatory gene expression during initial disease onset in Duchenne muscular dystrophy. Long-term benefits of deflazacort treatment for boys with Duchenne muscular dystrophy in their second decade.
Diagnosis and management of Duchenne muscular dystrophy, part 1: diagnosis, and pharmacological and psychosocial management. Treatments for muscular dystrophy: increased treatment options for Duchenne and related muscular dystropies.
Towards developing standard operating procedures for pre-clinical testing in the mdx mouse model of Duchenne muscular dystrophy.
Creatine supplementation reduces skeletal muscle degeneration and enhances mitochondrial function in mdx mice.
Measurement of sub-membrane [Ca(2+)] in adult myofibers and cytosolic [Ca(2+)] in myotubes from normal and mdx mice using the Ca(2+) indicator FFP-18. Muscle wasting in muscular dystrophy: decreased protein synthesis or increased degradation?
CINRG randomized controlled trial of creatine and glutamine in Duchenne muscular dystrophy.
Creatine monohydrate enhances strength and body composition in Duchenne muscular dystrophy.
Enhanced dystrophic progression in mdx mice by exercise and beneficial effects of taurine and insulin-like growth factor-1.
Nutritional therapy improves function and complements corticosteroid intervention in mdx mice. Evaluation of Potential Synergistic Action of a Combined Treatment with Alpha-Methyl-Prednisolone and Taurine on the Mdx Mouse Model of Duchenne Muscular Dystrophy. Implications of cross-talk between tumour necrosis factor and insulin-like growth factor-1 signalling in skeletal muscle. Damage and inflammation in muscular dystrophy: potential implications and relationships with autoimmune myositis. The inflammatory syndrome: the role of adipose tissue cytokines in metabolic disorders linked to obesity. Reduced necrosis of dystrophic muscle by depletion of host neutrophils, or blocking TNFalpha function with Etanercept in mdx mice.
Cromolyn administration (to block mast cell degranulation) reduces necrosis of dystrophic muscle in mdx mice.
2011.Spurney CF, Gordish-Dressman H, Guerron AD, Sali A, Pandey GS, Rawat R, Van Der Meulen JH, Cha HJ, Pistilli EE, Partridge TA, Hoffman EP, and Nagaraju K.
Preclinical drug trials in the mdx mouse: Assessment of reliable and sensitive outcome measures. Hypertrophic response of Duchenne and limb-girdle muscular dystrophies is associated with activation of Akt pathway. Electron microscopic and autoradiographic characterization of hindlimb muscle regeneration in the mdx mouse. Of bears, frogs, meat, mice and men: complexity of factors affecting skeletal muscle mass and fat. Regulation of skeletal muscle physiology and metabolism by peroxisome proliferator-activated receptor delta. Blockade of TNF in vivo using cV1q antibody reduces contractile dysfunction of skeletal muscle in response to eccentric exercise in dystrophic mdx and normal mice. PGC-1alpha regulates the neuromuscular junction program and ameliorates Duchenne muscular dystrophy.

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