Category Archives: Diet And Food

This low calorie diet should not be followed for more than 12 continuous weeks

THE Cambridge diet is popular with those looking for rapid weight loss, thanks to its strict structure andlow calorie products.

Users consume shakes, soups and bars that have been specially tailored to their weight loss goals.

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The Cambridge diet was developed by Dr Alan Howard at Cambridge University in the 1970s, and was launched as a commercial product in the US in 1980 followed by the UK in 1984.

It involves followers buying a range of meal-replacement products which are said to promote rapid weight loss.

Users can choose from six flexible diet plans ranging from 415 calories to 1,500 calories or more a day, depending on your weight loss goal.

The bars, soups, porridge and shakes can be used as your sole source of nutrition or together with low-calorie regular meals.

Depending on your products, weekly cost are around 48.30 but can be as low as 2.30 per meal for three meals.

A very low calorie diet that involves eating 1,000 calories a day or fewer should not be followed for more than 12 continuous weeks without a break.

If you are eating fewer than 600 calories a day, you should have medical supervision and there are protocols in place that your Cambridge consultant must follow to ensure this is sought.

Initial side effects can include bad breath, a dry mouth, tiredness, dizziness, insomnia, nausea and constipation from cutting down on carbs and fibre.

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The diet can only be done by getting in touch with aCambridge Weight Plan consultant, who weighs and measures you to determinewhich programmeis best for you and provides you with your chosen products.

Your consultant provides you with not only the products, but guidance and support as you progress with your diet and transition into maintenance.

The Cambridge products can be used on their own or used with regular meals for a more gradual weight loss.

Many feel that the plan is a short term option, as giving up normal meals and swapping them for a snack bar or a shake can be boring and feel socially isolating.

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Many people on very low calorie diets find the weight loss to be sudden and quite dramatic.

The meal replacements are all nutritionally balanced, so youre likely to be getting all the vitamins and minerals you need, albeit not from real food.

One woman who used the diet to drop five dresses sizes said the programme helped her to losea stone every four weeks and she slowly introduced healthy meals back into her diet.

While former Eastenders star and Loose Woman Martine McCutcheon has revealed she followed the Cambridge diet and losta stone in five weeks.

Martinerevealed that she decided to make a change in her life because she wanted to be healthy for her husband, Jack McManus, and their son, Rafferty, two.

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What is the Cambridge diet, is it safe, what foods are restricted and are there any success stories? - The Sun

Traci Mann is the keynote speaker at the free Crow Wing Energized Health and Wellness Summit Friday in Baxter. The summit is set from 7 a.m. to 1 p.m. Friday at Lakewood Evangelical Free Church, 6284 Fairview Road in Baxter. There are still seats available for the fourth annual health and wellness summit, which also provides a free continental breakfast and lunch.

Mann is a professor of psychology at the University of Minnesota. She has a doctorate in psychology from Stanford University and was a professor at UCLA before moving to Minnesota. Mann founded the Health and Eating Lab. Her biography notes her research has been used by the National Institutes of Health, the U.S. Department of Agriculture and NASA.

In her book "Secrets from the Eating Lab," Mann looks at a number of questions.

Is it my fault if my diet didn't work?

If I don't diet won't I gain a lot of weight?

Do I have less willpower than everyone else?

What is a reasonable goal weight?

Can I be healthy if I don't lose weight?

What are smart regulation strategies?

"Because diets don't work. And you don't need them to work, because you can be happy and healthy without dieting. Instead, we offer 12 smart regulation strategies that help you reach and maintain your leanest livable weightthe weight at the low end of your set range," Mann states on her website for the book. "These scientifically tested strategies work because they don't fight biology or rely on willpower. They don't require agonizing self-denial or a single-minded focus on your weight, so you can make these simple changes and then get on with the important things in life."

In addition to Mann's presentation, participants at the summit will hear from local success stories from those who took part in Crow Wing Energized lifestyle change classes. There will also be an opportunity to experience two of the nine breakout sessions:

Promoting health and movement in the workplace,

How Adverse Childhood Experiences can affect you over your Lifespan,

Follow the Money: Big tobacco at the local retail level,

It's a Matter of Balance,

Community Gardens: 'Healthy choices Inspire,'

Leaving a Legacy,

Eat Right when money's tight,

Gratitude ... How it can change your life,

Opportunities to be active in our communities.

With additional spaces still available for the health summit, Crow Wing Energized reported those who are already registered should feel free to invite others to attend with them, and those who haven't yet registered, still have the opportunity to do so. Go to http://www.crowwingenergized.org for more information on the summit or to register. Participants may find they can attend all or part of the session. On Friday, registration and continental breakfast begins at 7 a.m. with a welcome and history behind Crow Wing Energized at 8 a.m. and the keynote speaker slated to begin at 8:15 a.m. Breakout sessions begin shortly after 10 a.m. A noon lunch will include success stories of lifestyle changes followed by a wrap-up and question and answer period before the summit ends. Go to bit.ly/2qunrq5 for more details on the breakout sessions.

Original post:
Mann: Diets don't work, instead think smart strategies for weight loss - Brainerd Dispatch

Some types of feed additives developed to mitigate mycotoxins in feed for warm-blooded animals may be ineffective for fish, says new research.

A team of researchers at the University of Guelphs fish nutrition research laboratory examined the use of one type of commercially available feed additives to mitigate the mycotoxin deoxynivalenol (DON) in the diets of rainbow trout(oncorhynchus mykiss). The group published its research in the journal Aquaculture .

The objective of this study was, therefore, to investigate the potential efficacy of a commercial feed additive (CFA) with adsorbing and bio-transforming properties in minimizing or preventing the adverse effects of diets naturally contaminated with DON on growth performance and nutrient utilization of rainbow trout, said the researchers.

The team found that use of an absorbing and bio-transforming commercially available mitigation product in trout diets did not improve fish performance.

The feed additive used here was developed through extensive research and development with homeotherms; therefore, use in feeds for cold water fish species may be outside the scope of its effectiveness, they said. Additional work is essential to systematically develop novel approaches for mycotoxin mitigation in highly sensitive farmed fish species.

Mycotoxins are a group of naturally occurring metabolites generated by some fungi and that produce negative effects in human and animals when consumed, said the researchers. Mycotoxin contamination stems from fungal infection of feed crops and is linked to environmental conditions during different stages of production and storage.

In general, mycotoxins are not removed during a routine feed manufacturing progress, they said. The contaminants are often linked to unspecific symptoms ranging from reduced production to mortality, and sensitivity to mycotoxins tend to vary based on several factors including animal species and age.

It has been estimated that 25% of the world's crop production is contaminated with mycotoxins, said the researchers. The economic impact of mycotoxins is effectively impossible to quantify; however, risk assessment analyses have estimated that financial losses to US agriculture associated with crop losses, mitigation efforts and reduced livestock performance or mortality range from $630m to $2.5bn per annum.

Mycotoxins often considered in relation to animal health include aflatoxins, ochratoxins, fumonisins, zearalenone (ZON), they said. The group also includes a set of compounds called the trichothecenes, which includes deoxynivalenol.

The expanding use of plant-based ingredients in aqua feeds has increased the potential for farmed fish to face mycotoxin exposures, they said. In a survey of carp feeds, 80% of samples were found to have detectable amounts of DON.

Chronic feed-borne exposure to low doses of DON is commonly associated with anorexia (reduced feed intake and growth), decreased productivity and altered nutritional efficiency, said the researchers. Comparatively, acute, short-term exposure to higher concentrations of DON may result in leucocytosis, gastrointestinal hemorrhage, diarrhea and emesis or vomiting, particularly in pigs.

Several important finfish species are considered to be highly sensitive to DON, they said. The presence of the mycotoxins in trout feed has been linked to reduced weight gain, limited thermal-unit growth coefficient (TGC), limited feed intake and feed efficiency, along with reduction in carcass crude protein content, retained nitrogen, recovered energy, nitrogen retention efficiency and energy retention efficiency.

Feed additives are often used in feeds to mitigate the negative influence of mycotoxin presence, they said. Additives can be absorbing agents, like clay minerals or yeast cell wall extracts, or bio-transforming agents, such as bacteria, fungi, yeast and enzymes.

These products have been studied in several terrestrial, monogastric species, they said.

However, most of the work looking at mitigation products in fish feeds has examined the use of clay-based mineral products, they said. Little work has been done examining the use mycotoxin mitigation products that act through absorption or biotransformation.

In the study, 1,200 fish were given one of eight diets for a 12-week growth trial, said the researchers. The diets contained one of four levels of DON from naturally contaminated corn and were fed with or without the commercial feed additive (CFA).

Initial bodyweights were recorded and a sample of fish was collected to establish initial carcass composition, they said. During the study, feed intake was noted weekly and weights were taken every 28 days.

Fish were sampled at the end of the feeding trial to examine final carcass compositions, they said.

Diets, feed ingredients and fish tissues were checked for dry matter, ash, crude protein, lipids, gross energy content, they said. Growth rate, feed efficiency, retained nitrogen, recovered energy, nitrogen retention efficiency and energy retention efficiency were calculated.

Use of the CFA to mitigate the mycotoxin was not found to be effective, said the researchers. Mortality was not altered by the experimental diets.

Highly significant linear decreases in weight gain, feed intake and thermal-unit growth coefficient (TGC) were associated with increasing levels of DON in fish fed the diets with or without the CFA, they said.

Fish getting the contaminated feed showed loss of whole body crude protein, lipids, ash and gross energy content, they said. With increasing levels of DON in the feed, the fish also had increased water content and both linear and quadratic decreases in retained nitrogen, recovered energy, nitrogen retention efficiency and energy retention efficiency.

Inclusion of the CFA at the recommended rate (2 g/kg feed) did not minimize the adverse effects of diets containing increasing, graded levels of DON (up to 2.0 ppm) on growth performance, body composition or nutrient utilization of rainbow trout, said the researchers.

No significant interaction was noted between DON and the use of CFA in the fish diets, they said. Additional work is essential to systematically develop novel approaches for mycotoxin mitigation in highly sensitive farmed fish species, they added.

Source: Aquaculture

Title: Evaluation of the efficacy of a commercial feed additive against the adverse effects of feed-borne deoxynivalenol (DON) on the performance of rainbow trout (Oncorhynchus mykiss)

DOI:10.1016/j.aquaculture.2017.02.019

Authors: Jamie Hooft, Dominique Bureau

See the rest here:
Some mycotoxin mitigations may be less effective in fishfeed - FeedNavigator.com

Posted May 12, 2017, 6:45 am

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Have you heard of the blood type diet? I thought it had been debunked long ago but patients keep asking about it, so I figured I should learn more.

In 1996 Peter DAdamo, a naturopathic physician, published a book in which he described how people could be healthier, live longer, and achieve their ideal weight by eating according to their blood type. Ones choice of condiments, spices, and even exercise should depend on ones blood type. Soon, the book was a best seller and people everywhere were finding out their blood type, revising their grocery lists, and changing how they ate, exercised, and thought about their health.

Here are some of the recommendations according to the Eat Right for Your Type diet:

As mentioned, the recommendations for the blood type diets extend well beyond food choices. For example, people with type O blood are advised to choose high-intensity aerobic exercise and take supplements for their sensitive stomachs, while those with type A blood should choose low-intensity activities and include meditation as part of their routine.

High-quality studies about the blood type diet had not been published in peer-reviewed medical literature. Even now, a search in the medical literature for the authors name reveals no research pertaining to this diet. Studies published in 2013 and 2014 about the blood type diets are worth noting. The 2013 study analyzed the worlds medical literature and found no studies demonstrating benefit from a blood type diet. The 2014 study found that while people following any of the blood type diets had some improvement in certain cardiometabolic risk factors (such as cholesterol or blood pressure), those improvements were unrelated to blood type.

The theory behind this diet is that blood type is closely tied to our ability to digest certain types of foods, so that the proper diet will improve digestion, help maintain ideal body weight, increase energy levels, and prevent disease, including cancer and cardiovascular disease.

Type O was said to be the original ancestral blood type of the earliest humans who were hunter-gatherers, with diets that were high in animal protein. Group A was said to evolve when humans began to farm and had more vegetarian diets. Group B blood types were said to arise among nomadic tribes who consumed a lot of dairy products. And since Group AB blood was supposed to have evolved from the intermingling of people with types A and B blood, type AB recommendations were intermediate between those for people with types A and B blood.

Each of these theories has been challenged. For example, there is evidence that type A was actually the first blood group to evolve in humans, not type O. In addition, there is no proven connection between blood type and digestion. So, in addition to a lack of evidence that the diet works, serious questions remain about why it should work in the first place.

Its a fair question, especially since some improvements were seen in people who adopted certain blood type diets (see link above). Eating based on your blood type requires you to know your blood type and then follow a restrictive diet. Personal preferences might be a problem: a vegetarian with type O blood may struggle to stay on the assigned diet, and people who love red meat may be disappointed to learn they have type A blood. Recommended supplements are not cheap; neither are the recommended organic foods. And if you have certain health conditions, such as high cholesterol or diabetes, a nutritionist can make better evidence-based recommendations for you than those determined by your blood type.

Advocates of blood type diets may say that while the ideal study has not yet been performed, the absence of evidence doesnt prove theyre ineffective. And theres also no proof that these diets are harmful. So, my guess is that interest in the blood type diets will not disappear any time soon. But theres a reason that bookstores have rows and rows of books on diet, each claiming to be highly effective if not the best. We simply dont know which diet is best for each individual person. And even if we did, sticking to any single diet is often challenging.

Stand by its likely youll soon be hearing about yet another best diet. And my guess is that it wont have anything to do with your blood type.

Read more:
Diet not working? Maybe it's not your type - Harvard Health (blog)

Zoe Saldana has given up on dieting.

"I try not to deprive my body of anything because the moment I have just salads and protein for a few days, I crave carbs. But when I eat everything in balance, I think less about food and more about everything else. Its about eating to live, not living to eat," the 38-year-old actress told the June issue of Shape.

The "Guardians of the Galaxy" star focuses instead on eating clean.

"Its not that I like to eat superlight, just superclean. I like food that is fresh," she said. "I dont go for things that come in a can -- and Im losing trust in things that come in plastic."

She and her husband, Italian artist Marco Perego, like to prepare their own meals, choosing to eat more vegetables and less meat.

"My husband and I have been learning to cook with Asian spices, like turmeric, and ginger, and were having a blast," she said.

Diagnosed with Hashimotos thyroiditis in 2012, Saldana is motivated to eat clean in order to stay healthy.

"I know Ive become a very boring person to take to dinner, but Id rather be that way than deal with health issues," said the actress, who is gluten- and dairy-free, just like the rest of the family. "When you have an autoimmune condition, you have to stay away from foods that cause inflammation."

The busy mom of three boys -- twins Cy and Bowie, 2, and Zen, who she welcomed in February -- doesn't always have time to exercise either.

"I cant work out regularly, so I compensate by eating a lot healthier than I might otherwise," she said. "Once you have relatively healthy eating habits, your workout can become playing with your kids, strolling around the neighborhood, playing airplane, or just changing diapers."

After the birth of her twins, Saldana opened about the physical challenges of getting back into shape. Not only did the actress gain 70 pounds, but Saldana explained on Facebook that "everything from my thyroid to my platelets crashed" after giving birth.

Continue reading here:
Why Zoe Saldana doesn't believe in diets - ABC News

Several people have asked me for my thoughts on the recent Cell study that indicated a fasting-mimicking diet might stimulate beta cell regeneration. I finally found some time to read the study, and, while I hate to be a nay-sayer, Im not particularly optimistic. I present here a deep dive into the study. If youre not interested in the details, skip to the Conclusions section at the end.

The researchers set out to test the effect of a fasting mimicking diet on beta cell regeneration.

The fasting mimicking diet (FMD): a low-carbohydrate, low-protein, high-fat diet that results in similar changes in growth factors, glucose, and ketone bodies as seen with a water-only diet.

The researchers use a mouse model of T2D called db/db in which the gene for the leptin receptor is mutated. Leptin is a hormone produced by fat cells in the body, and when its receptor is mutated, mice do not properly regulate their appetites or hormones, resulting in obesity as well as increased leptin and insulin levels. Just as with human T2D, obesity in these mice leads to insulin resistance first, and, in later stages, beta cell failure. Despite these similarities, it is important to note that this is still just a model of diabetes, and not a perfect analogue. The symptoms of the human disease and the mouse model are similar, but the causes are very different. Notably, human T2D is not generally caused by leptin receptor mutations, or even a faulty leptin signaling pathway.

Nonetheless, in this study, the researchers let db/db mice develop diabetes (10 weeks of age), and then waited until the hyperglycemia had stabilized, indicating late-stage disease (12 weeks of age). At that point (14 days after hyperglycemia onset at 10 weeks), the mice were started on repeated cycles of FMD four days of FMD followed by 7 10 days of normal feeding. These cycles were continued for several months. The cycles of FMD led to substantially less hyperglycemia in the treated mice by 60 days after the start of hyperglycemia as compared to db/db mice on normal diets.

How did this happen? The authors claim that the cause is primarily increased beta cell function rather than increased insulin sensitivity. They show that plasma insulin levels are higher in the FMD-treated mice two weeks after beginning treatment, and the mice had more insulin-producing beta cells about four weeks after treatment. Further, those beta cells contained proteins considered to be markers for proliferation, indicating that the mice were seeing the effects of beta cell regeneration, rather than just increased beta cell survival.

These are very cool results, but lets pause here for a moment to be skeptical: first, let me remind you that this is a model of T2D that mimics the symptoms, but the underlying causes are quite different. Some research shows, for example, that beta cell dysfunction early on contributes to T2D, while in db/db mice, beta cell failure is a response to obesity and hyperglycemia, and the beta cells themselves are otherwise normal.

Second, it is important to note that the FMD-treated db/db mice weighed 25% less than the normally fed db/db mice. They were still about 20% heavier than normal, unmutated mice, but the weight loss here is important to consider. The reason that the db/db mice become hyperglycemic in the first place is that the leptin pathway is broken, leading to the mice eating too much, leading to obesity, which in turn leads to hyperglycemia and eventually beta cell failure. Its possible, then, that the real cause of beta cell salvation here is lessened obesity, not the diet itself. Whats the difference if the diet leads to lessened obesity? Well, causality matters here; if studies like this lead to us prescribing fasting mimicking diets, but the real cause of change is weight loss, then the diet alone will not necessarily lead to any changes. And, while the mice in this study saw weight loss, that is not a guarantee of the diet.

Those concerns aside, the beta cell regeneration is an interesting effect, and the researchers next decide to look at what happens in a mouse model of type 1 diabetes. For T1D, they use mice treated with streptozotocin (STZ). STZ is a beta cell toxin, so mice treated with the chemical lose their beta cells, resulting in hyperglycemia. This is considered a T1D model because, unlike the db/db mouse, obesity is not involved, and the mice are not insulin resistant. In other words, STZ mice lose beta cells first, then become hyperglycemic, whereas its the other way around for db/db mice.

Why did the researchers use STZ-treated mice rather than the most common T1D model, the NOD mouse? As with db/db mice, STZ treatment results in symptoms that look like T1D, but causes are very different. In human T1D, an autoimmune reaction to proteins of the beta cells results in the destruction of beta cells by the immune system. The NOD mouse similarly develops an autoimmune response to beta cells, and is therefore the more common model of disease. For this study, though, NOD mice, and human T1D for that matter, pose a big problem if FMD led to any beta cell regeneration, the immune system would likely just kill off the new beta cells, meaning the researchers wouldnt be able to see any of the regeneration even if it did happen. So, the researchers used STZ mice, which remove the immune response from the equation, focusing on the symptoms of T1D rather than the causes.

Researchers began cycles of FMD five days after STZ treatment. In this case, the cycles were 4 days of FMD followed by 3 days of normal feeding, and the cycles only continued for about 25 days. (Its not clear why this is different than with db/db mice; my guess, though, is that its practically easier for humans to work on weeklong cycles and they wanted results faster, but I dont have any evidence for that guess.) The researchers saw glucose levels return to near normal values about three weeks after starting the FMD treatment, and, as with the db/db mice, the STZ mice showed higher levels of plasma insulin as well as increased numbers of beta cells in the pancreas. A greater percentage of the insulin-producing cells also contained protein markers for proliferation, indicating that the FMD treatment was leading to beta cell regeneration, just as in the db/db mice.

Notably, this study is useful as a test of my skeptical claim above that weight loss rather than FMD resulted in beta cell regeneration. Here, the mice are not experiencing significant weight loss or weight gain, indicating that the effects seen are a result of cycling FMD. But, lets put our skeptic hats back on: I would argue that is the primary value of this study, as the relevance to T1D is minimal. Because there is no immune reaction at play, its entirely unclear what effect, in any, FMD would have on a model of type 1 diabetes in which the beta cells are either under attack in early stages of the disease, or later when there are no functioning beta cells left.

And, a nitpick: the researchers claim that FMD cycles also reduced levels of immune signals associated with inflammation during beta cell damage. The evidence here is cherry-picked at best, and seems like a failure to correct for multiple hypothesis testing. This is presented as supporting evidence and not the key point, so I will let it go, but I suspect its an example of data massaging rather than a real effect.

The researchers next checked the effect of FMD cycles in normal, non-diabetic mice. Using normal mice allowed them to analyze the mice on tighter time scales, and also to isolate the effects of FMD from all the complicated symptoms of the disease models. Normal mice were fed on the fasting mimicking diet for four days, at which point samples were collected. Following the first four days, the mice ate normally, and samples were again collected after one day of normal feeding and after three days of normal feeding.

When looking at islet cells, researchers found that the four days of FMD led to a trend of decrease in the number and size of cells. Note that a trend here is journal-speak for not statistically significant, and though the box plots used in the paper show a decrease overall, the actual numbers shown in the supplemental figures are not very convincing. Also note that the researchers have switched from measuring beta cells to measuring islet cells, which includes both insulin-producing beta cells and glucagon producing alpha cells. This is because, as the supplemental figures show, the trend in beta cells is even less convincing.

Lets take it at face value for a moment, and assume there really is a decrease in islet cells. Then, when researchers measure again after one and three days of normal feeding, it appears that the islet cells have returned, with more insulin- and glucagon- producing cells visible in the pancreas. The beta cells show increased presence of protein markers for cell proliferation, and there is an increased number of cells that appear to be in a transitional state, showing both alpha- and beta-cell markers. After three days of normal feeding, beta cells returned to pre-FMD levels.

The researchers next tried to establish what genes were contributing to this increased proliferation and transition to beta cells. They show significant changes in a handful of genes that have been previously shown to be relevant to lineage determination (that is, the process of going from stem-like ancestors of alpha and beta cells, called progenitor cells, to the fully-functional alpha and beta cells) in pancreatic islets.

But, but, but: I have some major statistical issues to pick with this part of the study. The genes they show are a set that happen to match the pattern they are looking for, but even then, some change insignificantly, and the others are assigned a p-value of less than 0.05 but more than 0.01. Knowing how science works, the researchers almost certainly checked a larger panel of genes than those shown, and presumably then picked out the ones that matched the expected pattern. I am almost guessing here, but its unlikely that the genes shown are really the only ones tried. And if thats the case, the p-values should be adjusted for multiple hypothesis testing, which would render the differences shown insignificant.

In which case, I would argue that there is a possible explanation for what the researchers are seeing that doesnt require beta cell regeneration at all: the period of deprivation during the FMD cycle leads to temporary shutdown of the hormone production programs in alpha and beta cells. As FMD is ended and normal feeding resumes, the increased availability of nutrients allows the cells to turn protein production back on, but the sudden commencement of activation signals throughout the cell also turns on some unintended genes that reflect the previous lineage of the cells. In metaphorical terms, the alpha and beta cells are like new college students from restrictive homes they go a little bit wild. After a few days of normal feeding, the cells re-stabilize, and return to normal levels of hormone production, maybe even over-producing glucagon and insulin for a while.

This interpretation fits with the data shown so far; the proliferation and progenitor marker proteins dont indicate real beta cell regeneration so much as quiet beta cells returning to full functionality. This would also explain why both alpha and beta cells seem to go quiet during FMD, but only beta cells subsequently express proliferation markers. The researchers claim only the beta cells regenerate, but that leaves the alpha cell disappearance and re-emergence unexplained. In the model I propose, both types of cells are shut off temporarily, and, when they wake back up, they enable a slightly different set of accidental genes.

How would one test this? You would want to show that the new beta cells did not exist prior to the period of FMD, and were split from progenitor cells only after normal feeding had begun. The authors do whats called a lineage tracing experiment, but this only serves to show that the protein markers for progenitor cells appear after the FMD treatment. In my model, this would still be the case the same beta cells go a little crazy and make progenitor markers, but that doesnt mean they actually become progenitor cells that generate new beta cells. So, while I dont have specific evidence for the alternate model, the current study has not ruled it out in my mind, which I dont fully buy the claim of beta cell regeneration versus just beta cell suppression followed by over-excitement.

But who cares about mice anyhow? There are an infinity of ways to cure diabetes in mice that go nowhere in humans. (My personal favorite: inject leptin straight into the brain.) Murine beta cells have been shown to be more capable of regeneration than human beta cells to begin with, and even a little bit of added insulin sensitivity in mouse models of diabetes can rescue the mice.

So the researchers next looked at human pancreatic cells. Specifically, they cultured pancreatic cells from non-diabetic and type 1 diabeticdonors. First, they cultured the cells in a dish with serum derived from clinical trial patients that were on a five-day FMD. The serum itself had less glucose and lower levels of growth factors than serum from humans on a normal diet, which is consistent with the expected effects on glucose and growth factors in the blood of fasting patients.

When the pancreatic cells were treated with the two different types of serum, the researchers saw a trend towards increased progenitor markers in the pancreatic cells. As before, this trend means there were no statistically significant changes observed in the cells, indicating that the FMD serum was not having much of an effect, if any, on the treated cells.

The researchers then abandoned the real human serum, and instead treated the pancreatic cells with normal growth medium, which is typically 10% serum with high glucose, and a fasting-mimicking medium (STS), which had only 2% serum and low glucose. As with the real human serum, STS likely had lower concentrations of growth factors in addition to lower glucose levels. STS, as described, sounds equivalent to what is often called starvation media, which is frequently used in cell culturing experiments to set cells in a state of minimal activity before administering a treatment that researchers are interested in. The media is therefore not unusual, but researchers dont usually study cells during the starvation itself.

In any case, the researchers see an increase in insulin production from the starved pancreatic cells as compared to the normal pancreatic cells. They also see increased presence of some of the same progenitor markers that were seen in the mouse cells. Note that the researchers do not show any indication of proliferation, but rather increased overall production of the progenitor markers, which would be in line with my theory above that the nutrient starvation results in some amount of perversion of normal regulatory pathways in the cell, but not beta cell regeneration.

The researchers conclude that our study provides an example of a potent and coordinated dietary regulation of cell-fate determination with the potential to serve as a therapeutic intervention to treat diabetes and other degenerative diseases. In other words, they claim they have shown that a fasting-mimicking diet can reprogram and regenerate beta cells, possibly to the point of being an effective therapy.

What do I think? As discussed above, I think their interpretation is over-optimistic. From where Im sitting, they have shown that starvation can lead to genetic dysregulation at a cellular level, which is interesting, but more from a basic-research perspective than a medical one. In other words, I dont buy the claims of beta cell regeneration, and am very skeptical that any real insulin-production could be found in humans from this sort of treatment.

And thats all before we get to the standard caveats that it is very hard to translate treatments between mice and humans. The particular mouse models used here are only rough approximations of either type 1 or type 2 diabetes, and the human studies here are in cultured cells only.

Lets assume for a minute, though, that they correctly interpreted the results, and a fasting-mimicking diet leads to some amount of beta cell reprogramming and regeneration. Would I then believe that there was a viable therapy here?

Lets consider the type 1 diabetes case first: it is not accidental that the researchers use a streptozotocin-induced model of type 1 diabetes rather than an immune-mediated model like the NOD mouse. In the NOD mouse, as in type 1 diabetic humans, even if the diet led to increased beta cell proliferation, those cells would quickly be killed off by the immune system, just as the original beta cells had.

What about newly-diagnosed type 1 diabetes? Isnt it worth trying, just for the chance? Frankly, its not clear this would help rather than hurt. The increased insulin production and the progenitor proteins that are showing up where they dont belong could lead to a more severe autoimmune reaction just as easily as a slower disease progression.

And for type 2 diabetes? Well, I actually suspect that this diet would help for many type 2 diabetics but only because you are almost certain to lose weight on a fasting-mimicking diet, and losing weight will ease the burden of insulin resistance for most type 2 diabetics. But this would be true of any diet that makes you lose weight, and if youre the kind of person who can commit to a fasting-mimicking diet for four days a week, then maybe you should consider a more moderate reduction in calories. That is more likely to be sustainable over the long term, and will probably be less exhausting and atrophying than a low-protein and low-carb diet. In other words, for type 2 diabetics, where the primary problem is insulin resistance, the effect of a fasting-mimicking diet is likely to be similar to that of any nutritionally questionable fad diet.

I started to conclude: In sum, if you really want to eat cod liver oil four days a week, go for it, but I will pass. Cod liver oil is what I imagine a low-protein and low-carbohydrate but high-fat diet to contain. But the study had an actual diet that they fed to the humans so I looked it up to determine what they actually ate. In the methods section of the paper, the researchers list: Human diet: Fasting mimicking diet (FMD) Propriety [sic] formulation belonging to L-Nutra. The paper goes on to describe the diet: The human version of the FMD is a propriety formulation belonging to L-Nutra. It is a plant-based diet designed to attain fasting-like effects on the serum levels of IGF-I, IGFBP1, glucose and ketone bodies while providing both macro- and micronutrients to minimize the burden of fasting and adverse effects (Brandhorst et al., 2015). Day 1 of the FMD supplies 4600 kJ [1099 calories] (11% protein, 46% fat, 43% carbohydrate), whereas days 2-5 provide 3000 kJ [717 calories] (9% protein, 44% fat, 47% carbohydrate) per day. The FMD comprises proprietary formulations of vegetable-based soups, energy bars, energy drinks, chip snacks, tea, and a supplement providing high levels of minerals, vitamins and essential fatty acids. Well, that sounds like an advertisement. I clicked through the provided link.

And, oh, look, its a 5-day meal box, all nicely packaged and marketed, complete with a modern-looking sans-serif font. Prolon, it says, Promoting health and Longevity [capitalization sic]. Well doesnt that sound homeopathic. A picture shows some of the foods contained in the box pretty, white packages of olives, minestrone blend, a food bar, and a handful of teas. The site goes on to describe the product: ProLon, [sic] is designed to promote the bodys natural ability to protect, regenerate and rejuvenate. In clinical studies, ProLon has been shown to reduce abdominal fat and maintain healthy levels of blood glucose, C-reactive protein (CRP), and insulin-like growth factor 1 (IGF-1). Unpublished clinical trials indicate that ProLon may have other positive health benefits.

And thats when I realized what was going on here. This paper, published in a very reputable scientific journal, is selling a fad diet. Well. Thats suspicious. I click through to the About pages of L-Nutra, trying to find the people involved, and, sure enough, the Chairman of the Board is Dr. Valter Longo, the corresponding author on the study. That seems like a significant conflict of interest.

I jump back to the paper, and look for the Disclosures section that often accompanies scientific papers. This one has none. But surely he disclosed the conflict of interest? Cell, like all major journals, (requires that authors disclose conflicts of interest). There it is, in the Acknowledgements, hidden away despite several mentions of the diet in question: V.D.L. has equity interest in L-Nutra, a company that develops medical food. All shares will be donated to charitable organizations.

All right, fine. So theres a conflict of interest, and its not well-disclosed. That doesnt by any means invalidate the study. But, it does make me suspicious, and even more skeptical than I was when I actually read the study.

So, I have a new conclusion sentence: In sum, proceed with caution. The science here has some holes, and someone stands profit off of the conclusions reached.

Read more from the original source:
The Questionable Effects of a Fasting-Mimicking Diet - A Sweet Life

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Evista and gluten-free diet - Evista blood clots stroke percentage - Avesta housing south portland maine - The Independent News

Priyanka Chopra might just be the Baywatch star having the most fun.

The actress plays a high-fashion, cut-throat power chickin the new film and that meant a pass on the series iconic red swimsuits.

You need to be on a diet of, like, one olive, she says with a laugh of her costars discipline.Im not like that as a person, you know? I like my food. During shooting, I could sit and eat whatever I wanted while everyone else was going to the gym.

Besides, I got to wear couture and heels on the beach, adds Chopra, 34, whose ABC drama Quantico was just renewed for a third season. Its so absurd that its fabulous.

FROM PEN:Amandla Stenbergs Best Beauty Lesson Is One We All Need to Follow

(Her trick for walking on sand in sky-high heels? Always walk on your toes.)

And the heels served another purpose, too: I asked for the highest of heels, because I couldnt be looking at Dwayne [The Rock Johnson] from down here and threatening him, right? I mean, I needed to look in his eyes.

Baywatch hits theaters this Friday.

Follow this link:
Priyanka Chopra Says She Did Not Diet or Exercise for Baywatch - PEOPLE.com

There are plenty of commercial diets that advocate cutting carbohydrates for instant weight loss and as a result, many Americans have become accustomed to counting the carbohydrate grams in the foods they eat and buy. The problem is our bodies need carbohydrate to function properly. So instead of avoiding this essential nutrient all together, make your carbohydrate work for you buy choosing foods that provide the nutrition needed for a healthy life.

In our bodies, carbohydrates are converted to glucose, our bodys main source of fuel. The brain, nervous system and blood cells all rely heavily on glucose to function properly. And while cutting out or cutting back on some carbohydrate heavy foods can be beneficial to your health (think pizza and donuts), there are many nutrient-dense carbs that have a place in your daily meal plan.

Choosing between simple and complex carbohydrates is the first step. Simple carbohydrates are exactly that: foods full of simple sugars that arent doing much for your body besides providing empty calories and probably tasting delicious. These foods, things like white bread, cookies and cakes, can have an occasional place in our diets, but in excess can contribute to weight gain, heart disease and diabetes.

Instead choose complex carbohydrates, which are foods that are minimally processed and deliver nutritional benefits like vitamins, minerals and fiber. Some great examples include whole grains, beans, fruits and vegetables. And yes, fruits and vegetables are carbohydrates.

Even though our bodies cant actually digest it, fiber is another important reason we need carbohydrates in our diet. Fiber helps regulate the bodys use of sugars, and appears to reduce the risk of developing many health conditions like digestive irregularities, heart disease and diabetes. A high-fiber diet is typically lower in calories and contributes bulk to your meals, making you feel full faster and longer. The daily recommendation is 25 grams for women and 38 grams for men. A diet high in plant-based foods can help you meet your daily fiber needs, so add extra vegetables to soups and casseroles, oats to meatloaf and breads, and top your yogurt or salad with fresh fruit.

The next time you are tempted to count carbohydrates, instead make your carbohydrates count by remembering the source is more important than the amount.

Taryn Palmer is a registered dietitian for the Magic Valley YMCA.

Read more here:
Palmer: Make your carbohydrates count - Twin Falls Times-News

May 17, 2017 by Adityarup

Certain kinds of foods prescribed to manage the rare metabolic disorder phenylketonuria (PKU) could contribute to skeletal fragility seen in many PKU patients, according to a new study by University of WisconsinMadison researchers.

Led by Waisman Center and College of Agricultural and Life Sciences investigator Denise Ney and her graduate student Bridget Stroup, the study represents the first human clinical trial to compare how different PKU-specific diets affect the bone health of people living with the disease. Skeletal fragility affects 40-to-50 percent of adults with PKU and 33 percent of children with the disease.

Individuals with PKU must adhere to a lifelong diet of medical foods that contain protein but are low in the amino acid phenylalanine. Their bodies are unable to metabolize phenylalanine, so it accumulates at high levels in their blood, leading to intellectual disabilities, seizures and other serious health problems.

However, almost all naturally occurring proteins contain phenylalanine, so in order to get enough protein, people with PKU have traditionally eaten medical foods containing synthetic protein substitutes made from amino acids. Still, they often struggle to maintain adequate bone health.

Just over a decade ago, Ney helped develop foods for PKU patients made from a protein called glycomacropeptide (GMP), a natural byproduct found in the whey extracted during cheese production. In one study, Ney showed that mice fed GMP-based diets had larger and stronger bones than mice on amino acid-based diets.

"It was a vital clue that there could be a link between amino acid medical foods and the skeletal fragility seen in many PKU patients," says Ney.

For the current study, published in the Journal of Nutrition and Metabolism, Ney and her research team assigned eight individuals with PKU to a diet of amino acid-based medical foods. Then, these same patients switched to a GMP-based diet.

The researchers found that, compared to when on the GMP diet, PKU patients had higher amounts of calcium and magnesium in their urine while on the amino acid-based diet, which indicated that their bones were leaching elements critical for bone health.

"The amino acid medical foods have high acid loads, which can change the overall acid-base balance within the body," says Stroup. Bones are able to buffer high acid loads in the body, but over time this leads to a breakdown and release of minerals. GMP medical foods, on the other hand, do not have high acid loads.

Although the researchers did not directly measure bone breakdown and density in this study, other studies have found that reducing the acid content of diets leads to lower urine-calcium excretion and increased bone density. The findings, Ney says, could help patients with other kinds of metabolic disorders, like maple syrup urine disease. And though the sample size of the study was relatively small, it is typical of rare diseases. Ney hopes to secure additional funding for further study.

Her work carries on a legacy of PKU research at the Waisman Center and at UWMadison. Harry Waisman, after whom the center is named, championed mandatory newborn screening for PKU and dedicated his life to developing treatments for the disorder. Waisman was among the first to show that PKU can be managed by strictly adhering to a low-phenylalanine diet.

Today, Ney is working on a larger clinical trial to study the metabolism of calcium and other minerals in PKU patients consuming amino acid or GMP medical foods. "We will be looking at bone health, but also other physiological aspects, such as the gut microbiota," says Ney.

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Certain kinds of foods prescribed to manage the rare metabolic disorder phenylketonuria (PKU) could contribute to skeletal fragility seen in many PKU patients, according to a new study by University of WisconsinMadison ...

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New clues to healthy bones for those with PKU - Medical Xpress