Diabetics live longer with physical exercise

Exercise reduces your chances of developing type-2 diabetes, but even if you already have diabetes exercise is good for you. Definitely if you exercise for longer than the daily half hour that is advised.

At the Lawrence Berkeley National Laboratory, the biostatistician Paul Williams examined data gathered in the National Walkers’ and Runners’ Health Studies. In that project researchers have been following several hundred thousand runners and walkers since the twentieth century – and among them are 2160 men and women who take medication for diabetes.

Williams knew how often the participants walked and ran, and divided them into three groups on the basis of the amount of calories they burned. The first group did the equivalent of 1.07 MET-hours per day. 1 MET-hour is the equivalent of about 1 km running or 1.5 km walking at a brisk pace.

The second group did between 1.07 and 1.8 MET-hours a day. If you manage the 1.8 MET-hours per day, you do exactly the amount of exercise that health experts advise. That means walking briskly for a good half hour every day.

The third group that Williams separated out were those who did more than the 1.8 MET-hours per day, and thus got more exercise than advised.

When Williams then looked at which diabetics had died, he saw that their mortality risk was lower, the higher their MET-hour figure was. In the figure below the mortality risk of the diabetics category with the least exercise.

Diabetics are more likely to die, and this is mainly because the disease damages the heart and blood vessels. Williams discovered that walking and running reduced the risk of dying from cardiovascular disease. In addition, exercise also reduced the chance of dying from an infectious disease or a kidney disease.

“Most people at risk for diabetes are not sufficiently active as defined by the recommendations for the general population, little less the recommendations for diabetic patients”, Williams concludes. “These results identify important additional benefits for diabetic patients to exceed the current general physical activity recommendations for adults.

Reduced Total and Cause-Specific Mortality from Walking and Running in Diabetes

This study aimed to assess the relationships of running and walking to mortality in diabetic subjects.

We studied the mortality surveillance between January 1, 1989 and December 31, 2008, of 2160 participants of the National Walkers’ and Runners’ Health Studies who reported using diabetic medications at baseline. Hazard ratios (HR) and 95% confidence intervals (95% CI) were obtained from Cox proportional hazard analyses for mortality versus exercise energy expenditure (MET-hours per day, 1 MET·h ?1-km run or a 1.5-km brisk walk).

Three hundred and thirty-one diabetic individuals died during a 9.8-yr average follow-up. Merely meeting the current exercise recommendations was not associated with lower all-cause mortality (P = 0.61), whereas exceeding the recommendations was associated with lower all-cause mortality (HR = 0.64, 95% CI = 0.49–0.82, P = 0.0005). Greater MET-hours per day ran or walked was associated with 40% lower risk for all chronic kidney disease-related deaths (HR = 0.60 per MET·h·d?1, 95% CI = 0.35–0.91, P = 0.02), 31% lower risk for all sepsis-related deaths (HR = 0.69, 0.47–0.94, P = 0.01), and 31% lower risk for all pneumonia and influenza-related deaths (HR = 0.69, 95% CI = 0.45–0.97, P = 0.03). Running or walking ?1.8 MET·h·d?1 was associated with 57% reduction in cardiovascular disease (CVD) as an underlying cause of death and 46% lower risk for all CVD-related deaths versus <1 .07="" d="" h="" met="" nbsp="" p="">
All results remained significant:

1. adjusted for baseline BMI and 
2. excluding all deaths within 3 yr of baseline.

These results suggest that

1.  exercise is associated with significantly lower all-cause, CVD, chronic kidney disease, sepsis, and pneumonia, and influenza mortality in diabetic patients and:
2. higher exercise standards may be warranted for diabetic patients than currently provided to the general population.

Muscle mass extends life expectancy

If you do heavy physical work or weight training, you’ll not only make your body more muscled and stronger, but you’ll also make it last longer.

Researchers used to think that overweight elderly people had a higher risk of dying, but recent studies have shown that both overweight and underweight elderly people are more likely to die. More and more epidemiologists are therefore coming to the conclusion that it’s not bodyweight that determines how long you are likely to live, but lean body mass.

In other words: the muscles.

Preethi Srikanthan tested this theory by examining data on 3695 over 55s gathered for the National Health and Nutrition Examination Survey III. Srikanthan followed the participants from the period 1989-1994 until 2004. When the study started the men were over 55 and the women older than 65. Srikanthan noted which of the participants died in the 10-16-year period.

There was no relationship between the participants’ amount of non-muscle mass and their survival chances, Srikanthan discovered when he divided the participants into four equal-sized groups (quartiles) on the basis of their non-muscle mass, and then calculated their mortality risk.

But when Srikanthan divided the participants into quartiles based on muscle mass, he did find a relationship. Participants with lots of muscle mass were 20 percent less likely to die than participants with little muscle mass. Srikanthan is not sure how muscle mass increases our survival chances. Perhaps it protects against high glucose levels, perhaps it reduces the amount of dangerous fat in the body, or perhaps muscles produce protective substances. But he does have a word of advice. “Get up and start moving”, the researcher said.

Clinical study to assess the efficacy and safety of a citrus polyphenolic extract of red orange, grapefruit, and orange on weight management and metabolic parameters in healthy overweight individuals.

Gynecomastia: Causes & Cures

Out of all the side effects a steroid user could potentially experience, gynecomastia (aka bitch tits) is one of the worst…and it certainly tops the list when it comes to cosmetic side effects. Being heavily associated with womanhood, the very nature of this side effect is an affront to our masculinity. Not only is it embarrassing, but in some cases it can destroy the entire appearance of one’s physique. We have all seen pictures of the more extreme cases, where the  bodybuilder literally looks like he has grown a small pair of tits on an otherwise normal body. The severity of this condition can range from only slight swelling, which is often imperceptible from a visual standpoint, to the more extreme cases, as mentioned above Fortunately, gynecomastia does not develop over night and its progression is easily halted and reversed if the proper steps are taken in a timely fashion. There really isn’t any good excuse for a steroid user to experience permanent, visible breast tissue growth. Those that do either don’t care or rather (and much more likely), they weren’t prepared and/or educated to deal with this side effect ahead of time. While there are numerous potential causes of this condition, the  bodybuilder generally only has to worry about a few of them and the available treatment options are simple in their application. Through minimal self-education and a small financial investment we have all the tools we need to keep this side effect at bay.

The most important factor in the prevention of gyno is knowing how it occurs in the first place. Since this article is targeted mainly towards the steroid-using bodybuilder, we will only address the causes which are directly attributable to PED usage. There are 4 types of steroids which can cause gynecomastia , the most prominent of which are the aromatizable steroids. Aromatizable steroids are those anabolic sterods which are capable of converting to estrogen. This includes many steroids, such as Testosterone, Methyltestosterone, Methandrostanolone (Dianabol), and to a lesser degree, Nandrolone (Deca), and Boldenone (EQ). This conversion process is initiated when aromatizable anabolic steroids interact with aromatase, which is an enzyme necessary for the biosynthesis of estrogen. See below for a depiction of this interaction:

When low dosages of these steroids are administered, the degree of conversion is not sufficient to cause this side effect. However, this threshold is regularly crossed by BB’rs who utilize dosages well in excess of those required to avoid estrogenic side effects. The problem with being able to pin-point the dose at which this side effect occurs is that not all individuals are affected equally by the same dose. Some can get away with using fairly large dosages of highly aromatizing drugs, such as testosterone, while others seem to develop problems even with minimal use. I know a powerlifter who was able to use a full gram of pharmaceutical-grade testosterone per week without experiencing any gyno symptoms, while other people have encountered early signs of gynecomastia at only 250 mg weekly. For this reason, assumptions should not be made beforehand regarding personal tolerance. When it comes to learning your limit, real-world experience must be your teacher. However, if I had to guess, I would say that most individuals will begin to experience the early stages of gyno by the time they reach 400-500 mg per week when using testosterone, assuming preventative action is not taken.

The 2nd type of steroid which can potentially cause gyno are those which appear to exhibit inherent estrogenic activity, despite lacking the ability to aromatize. One example would be Oxymetholone (Anadrol). This steroid is not capable of converting to estrogen to any degree, yet it causes gyno in a moderate percentage of users. The most plausible explanation for this side effect is that the Anadrol molecule itself demonstrates estrogenic activity, likely by attaching directly to the estrogen receptor. While we cannot yet conclusively state this to be fact, it seems more probable than the other theories which have been put forward over the years.

The 3rd type of anabolic sterods associated with the development of gynecomastia are the progestin-based steroids, which promote their effects through direct stimulation of the progesterone receptor. Two examples which fit this description would be trenbolone and nandrolone. However, these drugs differ from the previously mentioned anabolic sterods  in that they rarely cause gyno on their own. Typically, they require the presence of estrogen (usually at above normal levels) in order to have an impact on the growth of breast tissue. In essence, their progestagenic effects tend to exacerbate the effect of estrogen, thereby acting more as a contributor rather than the primary offender.

The last category of AAS with a history of exhibiting this side effect are those which result in estrogen-rebound. Anticipating the effects of these drugs can be difficult, as they are much less predictable in their behavior. Not only does personal response vary tremendously between individuals, but there is often a lack of consistency even among the same individual. For example, a particular steroid may be employed multiple times without incident, only to cause troubling gyno symptoms under nearly identical circumstances at a later date.

We’ve looked at particular types of anabolic sterods and how they work to cause gyno, but there are other causes which should not be overlooked, one of which is an out of balance androgen to estrogen ratio. DHT itself, as well as many DHT derivatives, possess natural anti-estrogenic activity. Therefore, even in the face of stable estrogen levels, a reduction in these hormones may lead to the appearance of estrogenic side effects. In turn, an increase in DHT or its related metabolites will enable an individual to more effectively deal with increased levels of estrogen. This is why a steroid user is much more likely to encounter estrogenic side effects using testosterone alone, compared to a combination of testosterone and Drostanolone (Masteron), which was developed specifically for the management of female breast cancer.

The last cause of gyno in the steroid user is prolactinemia, which is an elevation of prolactin levels outside of the normally recognized limits. The most common cause of prolactinemia in the general population is prolactinoma (tumor of the pituitary gland), although this condition can be caused by administering prolactin elevating steroids, such as trenbolone and nandrolone. However, just like progesterone, prolactin rarely causes gyno by itself. This is not because prolactin is not able to accomplish this. Rather, anabolic sterods generally aren’t able to elicit elevations in prolactin adequate for causation. Most of the time, prolactin acts to exacerbate the effects of estrogen (similar to progesterone), making it a contributing factor and not the primary cause in the large majority of cases. Still, there have been instances in which these steroids were able to cause gyno and/or lactation independent of aromatizable anabolic sterods. I want to emphasize the fact that lactation rarely occurs in steroid users, but when it does, it is almost always attributable to excessive dosing with the offending steroids, in combination with poor personal response.

The Cure

Once you’ve indentified the root of the problem, deciding on the best course of action is relatively simple. With that said, let’s get right to the nuts-n-bolts of how to get rid of gyno. When excess estrogen levels are the culprit (aromatizable anabolic sterods), there are multiple treatment methods available to us. Ideally, you want to stop the problem before it even begins. Therefore, when planning your cycle, if you know you will be using a dose of aromatizable drugs likely to raise estrogen into a problematic range, the concomitant administration of an A.I. (anti-aromatase) from the outset of your cycle is the best bet. By making an A.I. an integral component of your program right from the start, you will never find yourself in an emergency situation.

While A.I’s can be used in either the prevention or reversal of gyno symptoms, they are best employed as a preventative measure…and with good reason. You see, the job of an A.I. is to prevent testosterone from aromatizing into estrogen, which it does very well, but the problem is that it does absolutely nothing to prevent currently circulating estrogen from continuing to cause problems. As long as A.I’s are utilized as a preventative measure and not for the treatment of an emergency situation, they are preferable to other gyno remedies, but that is not all. The primary mechanism by which A.I’s inhibit gyno formation (management of systematic estrogen) also provides numerous other benefits not found elsewhere, such as: reduced water retention, lowered blood pressure, decreased fat storage, and others. Lastly, A.I.’ do not reduce IGF-1 levels, as will Tamoxifen (Nolvadex).

Should you find yourself in a situation where gyno symptoms manifest unexpectedly, you should turn to Tamoxifen (Nolvadex) for assistance. Why? The body is programmed to convert a percentage of our naturally produced testosterone into estrogen. This is a necessary and healthy process, as estrogen is required for a variety of male physiological functions. However, as the dose of androgens continues to rise, the body continues to convert roughly the same amount of androgens into estrogen. This becomes a problem once we begin administering supraphysiological quantities of these drugs. The much greater amounts of estrogen now floating through the bloodstream are free to attach to any estrogen receptor sites they come in contact with, including those in breast tissue. The end result is gyno formation…also known as “growing boobs”. This is great in teenage girls, but not in grown men.

The only way to put an immediate stop to this is by deactivating estrogen in breast tissue. Tamoxifen does just that. Due to its greater binding affinity, Tamoxifen is able to dislocate estrogen from the receptor site and take its place, leaving the estrogen with nowhere to attach. The main downside of Tamoxifen relative to the A.I.’s, aside from its IGF-1 lowering effect, is that it is powerless to reduce systematic estrogen levels. Because whole-body estrogen levels remain elevated, the user is subject to side effects such as water retention, increased fat storage, increased blood pressure, etc.

The 3rd way to treat estrogen-induced gyno is through the use of anti-estrogenic steroids, such as Masteron or Proviron. Of this we can be certain, as Masteron has been proven effective, in a clinical setting, at modulating estrogen levels in breast tissue. In fact, Masteron was originally designed for use in women afflicted with breast cancer. Like A.I.’s, Masteron and gang work to keep estrogen levels low by preventing aromatization. As mentioned above, this is a decisive advantage compared to a drug like Tamoxifen, which is completely ineffective at managing whole-body estrogen. This also means it is best used as a preventative measure and not in emergency situations. As a whole, anti-estrogenic steroids are not as potent as the A.I’s. Therefore, these steroids should be utilized right from the start of a cycle, at a dosage commensurate to the amount of aromatizable drugs being used. In my opinion, Masteron is usually the best steroid for this purpose, as it not only provides an anti-estrogenic punch similar to Proviron, but it also increase the muscle-building value of a cycle, unlike Proviron, which has virtually no muscle building effect. Lastly, Masteron provides the additional benefit of enhanced sex drive.

We’ve spoken a lot on estrogen-induced gyno, but not all gyno is estrogen dependent. Prolactin has the ability to cause gyno if levels get high enough, as does progesterone. While anabolic sterods do not directly increase progesterone levels, some steroids themselves are progestins (ex. trenbolone & nandrolone), exhibiting progestagenic effects on the body. Generally, this progestagenic effect is not strong enough to cause gyno by itself, but it can certainly exacerbate the effects of estrogen, making the problem worse. In the same way, anabolic sterods are generally not able to increase prolactin high enough in order to cause gyno by itself, yet it can certainly contribute to the problem. In extreme cases, individuals using large doses of Trenbolone have been known to lactate. Although this is rare and typically only occurs in heavy users with an unfavorable response, it does occasionally happen.

The most effective treatment for normalizing prolactin levels are the anti-prolactin drugs, such as cabergoline, pramipexole, or bromocriptine. Bromocriptine is a 1st generation anti-prolactin drug. It is not as potent as the other two and since it is less specific in its actions, it comes with an increased risk of side effects. There is no longer any good reason to choose bromocriptine when seeking relief from elevated prolactin. While cabergoline and pramipexole will both get the job done, in terms of compatibility and ease of use, caber is usually preferred due to its reduced side effect profile and longer active life. If there is one downside, it would be its greater cost. Pramipexole must be dosed daily, while cabergoline is usually only administered once every 2-3 days, depending on need. As for the progestagenic effects of anabolic sterods, a stated above, gyno is rarely ever a concern as long as estrogen levels are properly managed. Therefore, no specific treatment is indicated. Rather, you indirectly treat the problem by maintaining a normal estrogen level.

That about sums it up, guys. If there is one take home message here, it is that prevention is preferable to correction. Stop gyno before it starts by keeping your estrogen level stable and it is very unlikely that you will ever have gyno issues. For those who are very sensitive to the effects of prolactin, yet like to use high doses of trenbolone or nandrolone, you may require the additional use of an anti-prolactin drug. However, most of us will not need these in order to avoid gyno.

Obviously, personal experience will play a key role in showing us what we can and cannot do as we attempt to stay gyno-free, so as you go about experimenting with different steroids & dosages, make sure you have the appropriate ancillaries on hand just in case they are needed. It is always wise to have a back-up supply of Tamoxifen lying around, simply because it’s almost universally effective for stopping gyno, regardless of the cause.

How to Protect the Liver During Anabolic Steroid Use

Q: “What can I do with my anabolic steroid cycle planning to help protect my liver?”

A: First, liver harm from anabolic steroids comes principally or entirely from alkylated anabolic steroids. Where the steroids are non-alkylated and estradiol levels remain normal, there’s almost never harm to the liver from steroid use. (A handful of apparent cases exist in the medical literature, so I don’t rule out that it could occur in very rare cases. Example non-alkylated steroids are testosterone, Masteron, Trenbolone, Boldenone (Equipoise), Nandrolone (Deca Durabolin), and Primobolan.

Keeping liver safety in mind, an effective cycle should have one or more of these steroids as the base, or even as the entirety of the cycle. About 350-700 mg/week of a steroid stack, though, may be an alkylated compound.

The most common alkylated steroids are Dianabol, Anadrol, oxandrolone (Anavar), and Winstrol. Alkylated steroid use is preferably limited to only six weeks at a time, though of course many who go longer don’t suffer lasting harm. However, sustained use of oral anabolic steroids absolutely can cause undetected formation of scar tissue in the liver. This effect can be cumulative, as the scar tissue does not heal. And thoroughly excellent gains can be achieved without “pushing” the 6-week rule.

If cycle length is greater than 6 weeks, then appropriate amounts of testosterone can substitute for the orals. I replace Anadrol or Winstrol with testosterone on a milligram for milligram basis. I replace Dianabol on a three-to-two basis, or in other words, 50 mg/day Dianabol is replaced by about 75 mg/day of testosterone. Oxandrolone, on the other hand, is replaced with Masteron on a three-to-two basis, or trenbolone on a two-to-three basis. Each period of alkylated steroid use should be followed by about twice as much time not using alkylated steroids, or longer. Estradiol preferably will be kept in the normal range, or not much above it, as elevated estradiol is slightly liver toxic. In and of itself estradiol toxicity is not greatly important, but in combination with alkylated steroid use, it adds to the toxicity.

Obviously hepatotoxic drugs and excessive alcohol use should be avoided, as should heavy use of NSAID’s, aspirin, or acetaminophen. Cautious use is fine. In terms of supplementation for liver health, lecithin may be taken in amounts such as 3-7 g/day together with B vitamins. With regard to milk thistle, steroid-induced cholestasis results from reduced activity of the bile salt export pump, and silymarin and silibinin (components of milk thistle) act at this point and can partially block the adverse effects of steroids. However, cheap milk thistle products don’t provide much of these substances. As for liver antioxidants, the problem does not seem to be one of oxidation and I don’t think they make a difference.

Liver protection supplementation may safely be omitted when the above principles are followed. Supplementation shouldn’t be a license to use alkylated steroids less carefully. I would treat supplementation only as a backup.

Food Addiction – A Serious Problem, Simple Solution

Food addiction is a very serious problem and one of the main reasons some people just can’t control themselves around certain foods, no matter how hard they try.\

Food addiction is, quite simply, being addicted to junk food in the same way as drug addicts are addicted to drugs. It involves the same areas in the brain, the same neurotransmitters and many of the symptoms are identical. Food addiction is a relatively new (and controversial) term and there are no good statistics available on how common it is. This is very similar to several other eating disorders, including binge eating disorder, compulsive overeating and having an “unhealthy” relationship with food.

Processed junk foods have a powerful effect on the “reward” centers in the brain, involving brain neurotransmitters like dopamine. The foods that seem to be the most problematic include typical “junk foods,” as well as foods that contain either sugar or wheat, or both. Food addiction is not about a lack of willpower or anything like that, it is caused by the intense dopamine signal “hijacking” the biochemistry of the brain. There are many studies that support the fact that food addiction is a real problem. The way this works is pretty complicated, but this short video explains it in human terms:
There is no blood test available to diagnose food addiction. Just like with other addictions, it is based on behavioral symptoms.

Here are 8 common symptoms that are typical of food addicts:

1. You frequently get cravings for certain foods, despite feeling full and having just finished a nutritious meal.
2. When you give in and start eating a food you were craving, you often find yourself eating much more than you intended to.
3. When you eat a food you were craving, you sometimes eat to the point of feeling excessively “stuffed.”
4. You often feel guilty after eating particular foods, yet find yourself eating them again soon after.
5. You sometimes make excuses in your head about why you should eat something that you are craving.
6. You have repeatedly tried to quit eating or setting rules (includes cheat meals/days) about certain foods, but been unsuccessful.
7. You often hide your consumption of unhealthy foods from others.
8. You feel unable to control your consumption of unhealthy foods, despite knowing that they are causing you physical harm (includes weight gain).

If you can relate to 4-5 of these, then you probably do have a serious problem with food. If you can relate to 6 or more, then you are most likely a food addict. Although the term “addiction” is often thrown around lightly, having true addiction is serious business.

Food addiction can cause physical harm. It can lead serious diseases like obesity, type 2 diabetes, heart disease, cancer, Alzheimer’s, arthritis and depression, to name a few. But you have even bigger reasons to quit than some unfamiliar disease in your distant future. Food addiction is also ruining your life… today. It breaks your self-esteem, makes you unhappy with your body and can make your life a living hell (like it did for me). The seriousness of being a food addict can not be overstated. This is a problem that ruins lives and kills people. Literally.

The most important lesson I have ever learned is called the law of addiction: “Administration of a drug to an addict will cause reestablishment of chemical dependence upon the addictive substance.” A former smoker who has a puff of a cigarette will become addicted again… instantly. An alcoholic who has a sip of beer will relapse, with all the horrible consequences that follow There is no way of getting around it. This is simply how addiction works. I am personally convinced that food addiction is no different. One bite of cake, one sip of coke, one “cheat” – that’s all it takes. Of course, we all need to eat something. Otherwise we’ll die of starvation. But no one needs to eat sugar, refined wheat flour or any of the modern junk foods that people tend to lose control over.

Most food addicts will never be able to eat junk food like “regular” people again. That’s the cold, hard truth. But if they manage to avoid the “trigger foods,” then they should be able to eat healthy and lose weight without problems. The truth is… complete abstinence is the only thing that reliably works against addiction. The sooner you accept that, the sooner you will recover. Although the “everything in moderation” message may work for some people, this advice is a complete disaster for food addicts. When it comes to addiction, moderation fails. Every time. This is the simple (but not easy) solution to addiction. Avoiding the addictive substance at all times.

Completely avoiding junk foods may seem impossible. These foods are everywhere and are a major part of our culture. But believe me… once you’ve made the decision to never eat them again, avoiding them actually becomes easier. When you’ve made a firm decision to avoid them completely, then there’s no need for you to justify anything in your head and the cravings may not even show up. Many people who have done this (including myself) don’t even get cravings anymore, not after they’ve made a profound decision to simply avoid this stuff… permanently.
But if you’re still in doubt and are unsure if this is worth the sacrifice, then write down a list of pros and cons.

Pros might include: I’ll lose weight, I’ll live longer, I’ll have more energy and feel better every day, etc.

Cons might include: I won’t be able to eat ice cream with my family, no cookies on Christmas, I might have to explain my food choices… (Most of these social dilemmas can be solved easily). Write everything down, no matter how peculiar or vain. Then put your two lists side by side and ask yourself: Is it worth it?

If the answer is a resounding “yes” – then you can rest assured that you are doing the right thing.

There are a few things you can do to prepare yourself and make the transition as easy as possible:

• Trigger Foods: Write down a list of the foods you tend to crave and/or binge on. These are the “trigger foods” you need to avoid completely.
• Fast Food Places: Write down a list of fast food places that serve healthy foods. This is important and can prevent a relapse when you find yourself hungry and not in the mood to cook.

What to Eat: Think about what foods you’re going to eat. Preferably healthy foods that you like and are already eating regularly.

Pros and Cons: Consider making several copies of your “pros and cons” list. Keep a copy in your kitchen, glove compartment and purse/wallet. Sometimes you will need a reminder about why you’re doing this.

It’s important to NOT go on a “diet.” Put weight loss on hold for at least 1-3 months.

Overcoming food addiction is hard enough as it is, by adding hunger and additional restrictions to the mix you will just make things even harder and set yourself up for failure.

Now… set a date, some time in the near future (maybe this weekend or next week).

From this day and onward, you will never touch the addictive foods again. Not a single bite, ever. Period.
When All Else Fails… Seek Help

If you end up relapsing and losing control over your consumption again, then you’re not alone.
Relapses are the rule when it comes to addiction, not the exception. Most people have a history of several failed attempts before they manage to succeed in the long run. That’s how it was for me and most recovering food addicts I know.

But if you relapse often, then there really is no point in trying to do it on your own again. If you’ve failed a hundred times, then the chances of you succeeding when you try it for the 101th time are almost nonexistent. Luckily, help is not far off… There are health professionals and support groups that can help you overcome this serious problem. You can seek professional help… for example from a psychologist or psychiatrist. Try to find someone who has actual experience in dealing with food addiction.

But there are several free options available as well, including 12 step programs like Overeaters Anonymous (OA), GreySheeters Anonymous (GSA) and Food Addicts Anonymous (FAA).  Food addiction is a problem that will rarely resolve on its own. Unless you deal with it, chances are that it will just get worse over time.

If you have this problem, then you have to do something about it now, or it will end up ruining your life.

Vitamin A derivative potentially treats type 2 diabetes, prevents its cardiovascular complications

 At a  time when obesity, type 2 diabetes, and their complications are a veritable epidemic worldwide, researchers at the University of Montreal and CHUM Research Centre (CRCHUM) recently demonstrated the potential of retinoic acid (RA), a derivative of Vitamin A, in treating obesity and type 2 diabetes and preventing their cardiovascular complications.

"In obese and insulin resistant mice, retinoic acid reduces the risk of cardiac apoptosis, stimulates the expression of cardio-protective genes reduced by the disease, and protects against the accumulation of collagen in the cardiac muscle, thus avoiding the occurrence of fibrosis and possible associated future complications," says the first author of the study, Daniel-Constantin Manolescu.

 Apoptosis is the process of programmed cell death. The discovery follows other research conducted by his team on the effects of RA on insulin resistance, diabetes, and obesity. "Blood glucose, insulin resistance, body weight, and adipocyte size were significantly decreased in treated animals, including abdominal fat, while dietary intake and physical activity were similar for treated or non-treated animals. This suggests an increase in basal energy expenditure," says Manolescu. White fat is an energy reserve formed by the accumulation of fat in the form of triglycerides to meet unexpected increases in energy costs, but it is also a hormonal tissue with a delicate balance. Overall, if energy intake is greater than expenditures over an extended period, obesity increases, while hormonal balance and energy metabolism are disturbed. In this context, resistance to type 2 diabetes develops over time.

Brown fat also stores triglycerides, but it has the ability to produce heat. Abundant in babies, brown fat does not disappear completely in adulthood. It is irrigated by blood vessels and has many mitochondria, the energy factories of cells. Vitamin A derivatives stimulate a mitochondrial uncoupling protein (UCP1) that allows uncoupling of the mitochondria pathway (oxidative phosphorylation ), which uses energy from the oxidation of nutrients for the production of adenosine triphosphate (ATP). For a period of time, they generate heat (thermogenesis) instead of ATP, which is traditionally the energy required for active metabolism. Exposure to cold leads to the stimulation of brown fat and white fat, promoting the conversion of triglycerides to free fatty acids and glycerol. However, in brown adipocytes, these fatty acids are rapidly oxidized in the mitochondria and produce heat (under the influence of the UCP1 protein). Brown fat thus helps to increase basal energy metabolism. As a result, hibernating mammals fatten in the fall without developing diabetes and lose weight without moving too much in the winter (while warming their den). They are also the animals that accumulate the most Vitamin A in their livers. Retinoic acid (a Vitamin A derivative) is recognized for its involvement in cell maturation and differentiation and may guide pre-adipocytes to become brown (or beige) instead of white. It is as if "boilers" were installed directly in reserves of white fat to melt it on the spot and prevent it from over-accumulating.

"Vitamine A is a bioactive nutrient. The originality of our project is in addressing obesity and type 2 diabetes through the involvement of retinoids. We have attracted international attention and were named among 12 teams in the world to bring conclusive data in this regard," says Dr. Pangala V. Bhat.

"Our studies on animals show that retinoic acid induces normalization of blood glucose and reduction of obesity. It is an important contribution to understanding RA action on the liver, fat, muscles, and the heart, and on retinoid metabolism, energy metabolism, fatty acid oxidation, and insulin resistance. Our research identifies new metabolic effects of retinoids and may lead to anti-obesity and anti-diabetic medicines," says Dr. Jean-Louis Chiasson.

Stress and Cortisol

We all get stressed from time to time and knowing how to deal with it is a lesson that everyone needs to learn. So what causes stress and why is it so bad for me? There are many reasons to avoid being stressed, but there is one substantial element that can cause your body to become a fat gaining machine. That element is called cortisol.

Cortisol is produced in the body when it`s faced with stressful conditions. Kids, family, work, school can all become stressful if preventative measures are not taken. When there is simply to much work to be done in a days time than what seems that can be done, your almost guaranteed to become stress. Stress is not the only cause of cortisol: overtraining, lack of sleep, and undereating can also make your body produce this harmful chemical. When your body is in a catabolic state, which simply means that your body doesn`t have enough nutrients to repair broken muscle fibers, cortisol will enter your body and try impairing you.

Fat gain and muscle loss will be the main problems your body has. You should also expect to suffer other side effects such as your body not getting the adequate nutrients it needs to function. Stress will not only have a negative impact on your bodybuilding, but will have an impact on your everyday life. Stess is often accompanied by physical symptoms, including: twitching or trembling, muscle tension, headaches, sweating, dry mouth, difficulty swallowing, abdominal pain (may be the only symptom of stress, especially in a child.) Sometimes other symptoms accompany anxiety: dizziness, rapid or irregular heart rate, rapid breathing, diarrhea or frequent need to urinate, fatigue, irritability, including loss of your temper.

Controlling cortisol is easier once you plan to stop it. The most important thing you can do is try keeping stress to a minimum. Sure, this is easier said than done but finding ways to eliminate stress is a step toward keeping cortisol to a minimum. In the gym, make sure you don`t overtrain. Your body easily becomes stressed by doing this. Finally, you should be eating enough protein in your diet to repair damaged muscle fiber that are broken down from the result of your training.

There are many products available that keep cortisol levels at bay, but following these techniques can save you money in the long run. The more time you spend educating yourself on proper ways of doing things, the better your body will be. You can either pop pills expecting a miracle with your body or you can use a method that has worked for hundreds of years, hard work!