Lose Weight And Look Great

Science now reveals that the foreign contents within your digestive tract play a dramatic role in your energy level, metabolic function, body weight, and cardiovascular health. While it is not the only causative factor involved in obesity and the metabolic syndrome, it is a significant contributing factor for virtually any overweight person – especially someone who has difficulty losing weight and keeping it off.

Researchers at Emory University School of Medicine¹ studied a mouse engineered to lack an important gene signal, Toll-like receptor 5 (TLR5), which helps recognize self-propelling bacteria. The lack of this gene signal caused the mouse to have an excessive appetite (eating 10% more than normal), develop insulin resistance, have high blood pressure, have elevated levels of cholesterol and triglycerides, develop fatty liver disease, and become 20% heavier than normal mice. In short, the mouse developed metabolic syndrome, an epidemic in America. The mouse was also at higher risk for developing ulcerative colitis and Crohn’s disease.

Researchers determined that the flora content, or microbiota of the intestinal tract was the source of the problem. Because the mouse lacks TLR5, the wrong type of bacteria overgrow in the stomach. Interestingly, when the researchers transferred the overgrown bacteria to normal mice they also developed metabolic syndrome abnormalities. This overgrowth of bacteria fueled obesity and triggered inappropriate food cravings in the mice. The mice did not get fat when food was restricted, yet insulin resistance persisted (a prerequisite to type II diabetes).

While over a thousand different kinds of bacteria naturally populate the digestive tract, there are two main classes: Firmicutes and Bacteroidetes. TLR5 mice have abnormal Firmicute populations, which cause the problem. 

“It has been assumed that the obesity epidemic in the developed world is driven by an increasingly sedentary lifestyle and the abundance of low-cost high-calorie foods,” says senior author Andrew Gewirtz, PhD, associate professor of pathology and laboratory medicine at Emory University School of Medicine. “However, our results suggest that excess caloric consumption is not only a result of undisciplined eating, but that intestinal bacteria contribute to changes in appetite and metabolism.”

Earlier Research on Firmicutes and Bacteroidetes

The famous mouse that makes no leptin hormone, the ob/ob mouse, eats endlessly and becomes extremely obese. This mouse has a 50% reduction in Bacteroidetes² and a proportional increase in Firmicutes. This means that the condition of obesity itself contributes to an excess number of Firmicutes. 

Through a variety of experiments with genetically altered mice, scientists now believe that excessive populations of the wrong type of Firmicutes activate enzymes that promote the storage of fat in fat cells (adipocytes). This means that activity in the gut has a direct impact on where calories go in the body.

Firmicutes are gram positive bacteria, many of which are friendly and essential to human digestion, such as Lactobacillus. On the other side of the Firmicute coin are members of the Streptococcus and Clostridium families, which are responsible for many infections. 

Chron’s, Bacterial LPS, and Obesity

In 2010, Chinese researchers³ released a report on 3.3 million microbial genes obtained from the fecal samples of 124 individuals from Denmark and Spain. The gene set is 150 times larger than the entire human genome. Over 99% of the genes are bacterial, indicating between 1,000 and 1,150 prevalent bacterial species. Each individual has at least 160 species, which are also largely shared. This is the first catalog of organisms found in the human digestive tract. 

In this preliminary work, researchers identified gene signals associated with obesity and Crohn’s disease. “Apart from helping you digest, these bacteria may also play a very important role in … diseases like Crohn’s disease, cancer, obesity,” said lead author Jun Wang, executive director of the Beijing Genomics Institute.

Wang and colleagues in China are working on a similar 120-sample study in Chinese hospitals. “There are four groups: obese diabetics, obese non-diabetics, lean diabetics and lean non-diabetics. And we found some interesting bugs related to each type of diabetes,” Wang said.

In other words, gene signals arising from populations of gut bacteria have a direct interaction with human metabolism – a dramatic finding.

Another aspect of this problem is that bacteria produce an endotoxin from the shedding of their cell wall called lipopolysaccharide (LPS). LPS is a commonly studied compound, as it reliably induces inflammation. Researchers have found that gut-derived bacterial LPS enters the bloodstream and directly triggers insulin resistance⁴, especially liver-related insulin resistance that typically accompanies type II diabetes. Furthermore, a chronic high-fat diet for four weeks raises LPS two to three times normal levels. It is also documented in obese women⁵ that LPS activates inflammation, setting the stage for metabolic disease.

Of great importance is the fact that LPS inhibits leptin from appropriately entering the brain⁶. LPS has been shown to raise blood levels of leptin, directly inducing leptin resistance. It also raises blood levels of triglycerides, which are the main known cause of leptin resistance at the blood-brain barrier. 

It has been demonstrated in overweight and obese children⁷ that a lack of friendly flora and an excess number of the Firmicute Staphylococcus aureus are common findings. 

Overweight women are known to have imbalanced microbiota with excess numbers of Firmicutes⁸ in the Clostridium and Staphylococcus families. This problem is aggravated during pregnancy when the mother’s immune system is down-regulated so as not to reject the fetus, leading to excessive weight gain during pregnancy. Furthermore, the mother’s microbiota pattern is typically passed to the child. Interestingly, women given friendly flora probiotic supplements in the first trimester of pregnancy⁹ had less abdominal fat one year after pregnancy.

Another study shows that probiotics inhibit the gram negative bacteria H. pylori¹⁰ and stop it from producing the toxic LPS that interferes with human metabolism.

Collectively, these studies show a clear path from the overgrowth of the wrong digestive bacteria to the creation of leptin-resistant and insulin-resistant obesity, which eventually leads to increased risk for type II diabetes and heart disease.

While killing Firmicutes with antibiotics does lessen the metabolic problems of TLR5-lacking mice, this would only encourage regrowth of equally bad if not worse Firmicutes in humans, while also encouraging the overgrowth of another anti-metabolic population, candida albicans, making the societal problem of antibiotic resistance and new superbugs even worse.

Rather, it appears that natural remedies are the front line of defense against this problem. This begins with a diet that promotes balanced digestion by avoiding excess fat, refined sugar, alcohol, and junk food. Encouraging growth of friendly flora with probiotic supplements (acidophilus) and prebiotic supplements (various types of fiber) is another very workable solution. 

There are also many natural compounds known to kill inappropriate gram positive bacteria in the digestive tract. Oregano oil, medium chain fatty acids, bovine colostrum, and bovine lactoferrin are just some examples of nature’s toolbox. These all have significant advantages over antibiotics, as they do not breed germ resistance or disturb beneficial flora. While helping to reduce surplus populations of undesirable bacteria, these compounds also reduce surplus populations of candida albicans – unlike antibiotic drugs that encourage candida albicans overgrowth.

It is always important to address the underlying cause of any digestive problem, not just cover it up with antacids that further induce undesirable bacterial overgrowth by reducing our front line of defense (stomach acid). Improving the digestive tract can also have a significant impact on metabolism, weight management, and cardiovascular health.

Maintaining the integrity of your joint cartilage is vital to your quality of life, ability to stay fit, participation in physical activities, and general anti-aging. While the extra weight from obesity places understandable stress on cartilage, a new study indicates that it also increases the risk for rapid cartilage loss, going beyond just the issue of mechanical pressure from extra weight.

This study builds evidence that obesity-induced inflammation is detrimental to health in many ways. The study involved 3,026 people, ages 50 – 79, at risk for osteoarthritis or with early x-ray evidence of the disease. During a 30-month follow up period, 20 percent of participants had slowly progressive cartilage loss, while 5.8 percent had rapid cartilage loss. For each one-unit increase in body mass index (BMI), the odds of rapid cartilage loss increased by 11 percent.

How to Improve Cartilage Health

It is always beneficial to use nutrients like hyaluronic acid, chondroitin sulfate, and glucosamine as raw materials to help build joint cartilage and improve joint lubrication. At the same time, it’s important to reduce factors that damage cartilage. Excess body weight is more than a little problem for cartilage health. I recommend following the 5 Rules of the Leptin Diet and incorporating nutrients such as DHA and tocotrienols to help turn down inflammation coming from excess fat cells.

New research confirms that the more sweets you eat the more likely it is that your tongue’s sweet sensors¹ are disturbed, causing you to eat even greater amounts of sweets just to get a satisfied sweet sensation.  Unfortunately, this craving for sweet pleasure is accompanied by eating too many calories in general and thus weight gain is likely.

We have known for some time that leptin receptors on your tongue go numb to the sweet taste.  Thus, the problem of general leptin resistance—tongue-specific leptin resistance—and extra sweet food consumption go hand-in-glove.  It is important to understand that these are powerful subconscious and misguided cravings, and they lock in extra calorie consumption that is adverse to your health.

Another study also shows that your gut senses the taste of sweets² just like your tongue does. This triggers the initial and appropriate release of insulin along with a satiety signal called glucagon-like peptide-1 (GLP-1).  If your tongue is out of sync with your gut then you simply eat too many carbohydrates or other sweets before you feel full.  On the other hand, if you use artificial sweeteners or no-calorie natural sweeteners then your tongue is further skewed and your gut doesn’t sense the sweet intake at all (the gut needs glucose).  This is why any added sweeteners mess up leptin and your diet.

One way to fix this problem is to go through sugar withdrawal, abstain from eating any sugar, and eat much less carbohydrates for a week or two.  Then when you reintroduce them at meals, carbohydrates and fruit will taste much sweeter to you than before and you’ll be able to eat less of them and still feel satisfied.  You can have a bite or two of a dessert at your main meal, but catch yourself if you start to get back into a pattern of large dessert eating or the desire to have something sweet during the day.

Also, train yourself to eat more vegetables that are bitter in nature.  This helps balance your system of taste, in turn making healthy carbohydrate choices taste sweeter. 

Nutrients in LeptiSlim help cut down your cravings for sweets based on the bitter herbs they contain.  Pine Nut Oil naturally raises glucagon-like peptide-1, which in turn stops your sweet cravings.  Use supplements as needed to help you stay in control of these urges – otherwise they might get the better of you!

A stunning thyroid study in the Archives of Internal Medicine¹shows that women whose TSH scores were in the high end of the normal range were at a 69 percent increased risk for cardiovascular death.

A similar trend in men was also present, but not statistically significant. The range for TSH scores is typically 0.50 to 3.5 mIU/L. Women in the lower end of this range had no increased heart disease risk. As the number increased the risk went up. Women in the middle of this range (1.5 – 2.4) had a 41 percent increased risk, while women in the higher end of the normal range (2.5 – 3.5) had a 69 percent increased risk.

TSH is the signal that comes from your subconscious brain (pituitary gland) telling your thyroid to get going. Scores in the normal range mean that the thyroid is responding to the TSH “phone call,” just not very well. This means doctors will not see these types of TSH scores as a thyroid problem that needs medication – but they are reflective of a metabolic problem that clearly increases the risk of death from heart disease.

What are women to do? Get their thyroid working better. TSH scores come down naturally when the rest of the body works more efficiently. Weight management is one key to the issue, as extra body fat clogs metabolism and forces TSH up. However, stress is another important issue—whether a person is overweight or not. Providing key nutrients that help activate T4 to its biologically active form of T3 is a key to solving this issue, as well as protecting your liver and thyroid gland from free radical damage.

Selenium is an essential nutrient that supports the health of the thyroid gland and assists the conversion of T4 to T3. Manganese and gugulipid help protect the liver and also support the conversion of T4 to T3. Coenzyme B vitamins and ashwagandha are helpful stress-busters.

The take-home message of this very important study is that you can maximize longevity by doing what you can to keep thyroid-related metabolism running efficiently. A thyroid that is struggling, for whatever reason, even if it isn’t “medically in trouble,” is still a sign to take action to preserve your health and well-being. A simple TSH test can tell you where you stand on this risk issue. Also, pay attention to signs of sluggish thyroid such as low afternoon energy, low body temperature, poor mood, lack of coordination, and difficulty losing weight.

The DHA component of fish oil is a potent brain support nutrient that is a vital building block for optimal cognitive function. Optimal thyroid function is also a key to healthy brain and cognitive function. An interesting study done at the Federal University of Rio de Janeiro shows that fish oil can help optimize the function of thyroid hormone within liver cells to burn fat.  We also know that when fat piles up in your blood (evidenced by elevated triglycerides), cognitive problems are more likely to occur.

This study helps make the point that thyroid function is more than just an amount of thyroxine, T4, produced by your thyroid gland or taken as a medication.  In recent writing I pointed out the importance of selenium for converting T4 to the biologically active form of thyroid hormone,T3, by your liver. This study says that if your cells have adequate DHA in them, then T3 is much more effective at burning fat. The synergy of function between T3 and fish oil results in better metabolism.

This study is especially interesting because I have seen many times over the years that individuals may need to get to fairly high doses of fish oil before weight loss kicks in, such as 2,000 – 3,000 mg. of DHA. (Getting this amount of DHA would require taking more than 10 grams of some fish oil products). 

In my early years I thought this was because the body just wouldn’t give up bad fat until you put enough good fat in it. Over the past decade I believed it was because at a certain level of DHA intake, white adipose tissue starts to work a lot better, which is true. Now from this study I can predict that a certain level of fish oil intake may be needed to optimize thyroid function within cells. It also means that if you take a lot of fish oil and eat well but your triglycerides are not coming down, then you should take a thyroid boosting supplement with selenium in it to better activate your T3.

DHA in particular, and fish oil in general, have been shown to have a powerful influence on the health and well-being of your stored fat, as well as other aspects of metabolism such as insulin resistance.  In a study working with obese leptin lacking mice¹, researchers demonstrated the precise novel ways in which fish oil can protect against obesity—even in an animal that had no choice but to become obese.

The fish oil raised the level of adiponectin in the white adipose tissue, which helped calm down inflammation within stored fat.  This study demonstrated that adiponectin also prevents insulin resistance and diabetes by improving how the liver can process sugar.

Collectively, these benefits resulted in a decline of excess fat building up in the liver – preventing the very serious metabolic problem of fatty liver known as NASH (nonalcoholic steatohepatitis).  It is important to understand that this protection occurred in an animal that literally had no choice but to become diseased from obesity; fish oil stopped the process of disease progression.  This is a rather amazing study.

Additionally, the researchers discovered that fish oil was further metabolized into novel metabolic signaling compounds called protectins and resolvins, which were involved in many of the protective benefits of the omega-3 fatty acids.  This is an interesting new area of research.

Scientists have discovered that protein turns on specialized brain cells that keep you awake, keep your metabolism humming along, and keep you motivated to accomplish goals. In contrast, carbohydrates, without enough protein, do not activate these brain cells, which may result in a tired head and body, and potential weight gain due to sluggish metabolism.

This research involves specialized cells in the command and control center of your subconscious brain (hypothalamus gland). These cells are called orexins and they feed a specific nerve network referred to as hypocretins. Protein turns them on and carbohydrates turn them off.

I explain this subject in my article, Teen Sleep Problems Lead to Depression & Drug Abuse. This article focuses on how this nerve network gets overheated, resulting in anxiety and nervousness during the day and trouble sleeping at night. It explains how pleasure/reward turns off the excess stimulation, and results in potential for addiction to anything, including drugs.

This new research focuses on the other side of the coin – what if this system is turned too low resulting in sleepiness during the day, sluggish metabolism, and a lack of motivation?

Clearly, we all want to be in the middle, where we feel properly energized and awake during the day, have normal drive to accomplish goals, attain rewards that have nothing to do with addictive tendencies, and sleep properly at night.

This is another angle on why protein at breakfast is extremely important. It not only gets your liver into metabolic gear, but we can now say it also gets your brain turned on. It also helps explain why high sugar snacks or high carbohydrate/low protein meals can make a person tired.  Too much sugar landing on these cells turns your head off. The researchers also found that when protein and carbohydrates were contained in the same meal, protein prevented the carbohydrates from binding to these cells.

There are many practical applications for this information. People who tend to be anxious and not sleep well will want to have low protein at dinner and higher carbohydrates, assisting the ability to go to sleep properly. Lunch can be a mix of protein and carbohydrates; the right mix for you means your head stays awake during the afternoon and you have some drive to get things done. If you don’t feel that way, you are probably eating too many carbohydrates. If you feel wired and anxious in the afternoon you may have had too much protein. In general, people who need to lose weight need more protein, especially at breakfast and lunch, and possibly at dinner, to keep their metabolism activated. If you get too much protein you might have trouble sleeping. One size does not fit all – so pay attention to what you are eating and how your energy level and motivational drive respond to different types of meals.

The gene signal AMPK (5’ adenosine monophosphate-activated protein kinase) is an important energy sensor at the cell level. When it activates, fats are burned for fuel. A study shows that one of the numerous metabolic benefits of green tea is that it turns on AMPK.

Researchers were trying to figure out why green tea lowers cholesterol, triglycerides, insulin, and leptin. Their gene study showed that green tea turns off the enzyme that assembles fat (fatty acid synthase) and turned on the gene that helps cells burn fat (AMPK).  When this mechanism is turned on, at least for part of the day, it will certainly help weight loss.

AMPK is turned off every time you eat, on purpose. This is because your body needs to store the calories you consume. Between meals, about three to four hours after your meal—especially if you are following the Five Rules of the Leptin Diet, AMPK will turn back on and start helping you burn fat. 

AMPK can also be turned on by two minutes of vigorous exercise. Try this in the middle of the afternoon if you tend to suffer from an afternoon power outage or snack compulsion. Taking green tea mid-morning and mid-afternoon would be ideal times to help you enhance this natural fat burning process.

The phrase “death by snacking” is not too far from the truth, especially if you are overweight and struggle to lose weight. Two studies confirm the dangers of snacking, something I have been adamant about since I wrote Mastering Leptin in 2002. 

Both studies appeared recently in the American Journal of Clinical Nutrition. The first followed 29,206 U.S. men who were free of metabolic disease for 16 years. The study found that skipping breakfast was associated with a 21 percent increased risk for developing type 2 diabetes, which is why The Leptin Diet tells you to start your metabolic engines with a high protein breakfast. This study also confirmed the relationship between a high BMI, snacking, and the risk for type 2 diabetes.

Another controlled human study found that snacking caused a loss of the ability to sense fullness, resulting in consumption of larger and larger snacks. Snacking appears to induce a repetitive strain injury to your taste and pleasure system, making them numb to normal intake. 

The more food you eat, the fatter you are likely to become, which is news to nobody. Figuring out how to feel satisfied on less food is the trick. This is why following the Five Rules of the Leptin Diet are so important.

When you do not have leptin working to your advantage, leptin entry into your brain is decreased, while leptin levels in your blood elevate; this problem is known as leptin resistance.  In addition to leptin, the other important hormone made by your fat is adiponectin. Both of these hormones are made in tandem when you are metabolically healthy. Once you develop leptin resistance, your adiponectin levels decline. This causes insulin resistance and increased risk for type 2 diabetes.

When you eat is just as important as what you eat. It isn’t just an issue of how many calories you consume; it is also an issue of how efficiently you can metabolize the calories you do consume. Eating in harmony with leptin is by far the best way to improve metabolic efficiency.

Cinnulin PF¹, a water-soluble extract of cinnamon, has been shown to improve the antioxidant status and lower the fasting glucose levels of obese pre-diabetic individuals.  Researchers at the U.S. Department of Agriculture continue to document the power of nutrition to help improve health problems faced by millions.

Study participants took 250 mg of Cinnulin PF twice a day for 12 weeks.  These individuals started the study with elevated fasting glucose levels but were not yet diabetic.  The researchers measured various parameters of antioxidant function, which demonstrates free radical distress – a factor known to interfere with healthy blood sugar metabolism.  The study showed that as Cinnulin PF improved the antioxidant status of the participants then their fasting blood sugar improved.

This human study builds on earlier research showing that water-soluble cinnamon is both a potent antioxidant as well as an excellent natural way to improve blood sugar metabolism.