Fat burning foods

Prepare these whole foods in a soup or salad with no processed oils and other processed foods. Whole foods are better absorbed with a side dish of veggies pickled prepared with apple cider vinegar and tsp of brown sugar.  Adding lemon in most of your dishes also facilitate absorption from the Vitamin C in lemons.  There is no secret among our movie stars who have a nutritionist beside them. Only whole foods and drinking coconut water or healthy beverage an hour before a meal.

Eat iron-rich foods  and copper food sources with Vitamin C at noon and in the afternoon dinner, eat calcium rich foods with omega 3, magnesium, potassium and Vitamin B and C for your metabolism to help you burn fat. These are copper and iron rich foods eaten in moderation:

  • 1) Beef liver. 3 oz: 14 mg (over 100% DV)
  • 2) Sunflower seeds. ¼ cup: 0.63 mg (31% DV)
  • 3) Lentils. 1 cup: 0.5mg (25% DV)
  • 4) Almonds. ¼ cup: 0.4 mg (20% DV)
  • 5) Dried apricots. 1 cup: 0.69mg (34% DV)
  • 6) Dark chocolate. 1 square: 0.9 mg (45% DV)
  • 7) Blackstrap molasses. …
  • 8) Asparagus.

Some of the best sources of vitamin B6 are poultry, seafood, bananas, leafy green vegetables such as spinach, potatoes and fortified cereals. Your diet should include 1.3 milligrams of B-6 daily to support new red blood cell growth.

Chicken, turkey, salmon and other fish including canned tuna packed in water are all excellent natural sources of niacin. Fortified cereals, legumes, peanuts, pasta and whole wheat also supply varying amounts.

Animal foods are the only natural source of vitamin B12, but many products, including soy products and cereals, are fortified with B12 so it is widely available in the food supply. Other good natural sources include shellfish, such as clams, mussels and crab, fin fish and beef. You need only a small amount of B-12 — 2.4 micrograms daily. This B-12 will boost red blood cell production and support your nervous system.

Liver and egg yolks are the richest dietary sources of biotin — a nutrient needed for a healthy metabolism — but fortunately this B vitamin is well distributed throughout the food supply, so it is unlikely that anyone eating a balanced, varied diet will experience a deficiency. Salmon, pork and avocado are good sources; most fruits and vegetables contain a little biotin, as do cheeses and grain foods.

Yogurt and avocado are both excellent sources of pantothenic acid, a vitamin needed for enzyme function, but it is also available in a wide variety of foods such as legumes including lentils and split peas, sweet potatoes, mushrooms and broccoli. Consume 5 milligrams daily.

Magnesium Rich Foods
1. Spinach
2. Pumpkin seeds
3. Broccoli
4. Almonds
5. Black Beans
6. Kidney Beans
7. Avocado
8. Peas
9. Dark Chocolate
10. Banana
11. Cashews
12. Flaxseed
13. Black-eyed Peas
14. Pollock Atlantic Fish
15. Peanut butter

Potassium Rich Foods
1. Baked Potato with skin
2. Spinach
3. Baked Sweet Potatoes
4. White Beans
5. Lima Beans
6. Avocado
7. Squash
8. Tomatoes
9. Salmon
10. Apricots
11. Pomegranate
12. Coconut Water
13. Banana
14. Mustard Greens
15. Carrots
16. Walnuts
17. Halibut

Omega-3 Rich Foods
1. Mackerel
2. Salmon
3. Cod Liver Oil
4. Walnuts
5. Flaxseeds
6. Tuna
7. Anchovies
8. Egg Yolks
9. Spinach
10. Mustard Oil
11. Blueberries
12. Avocados
13. Broccoli
14. Lettuce
15. Strawberries

Sucrose, gut bacteria, toxins, and muscle integrity

Visceral fat, genes, heart disease and how the stomach talks to the brain

Who is prone to visceral fat?

The tendency to accumulate visceral fat is governed by genetic, ethnic, and gender differences. For example, people who inherit two copies (one from each parent) of a mutation in a gene involved in fat metabolism are more likely to have higher amounts of visceral fat than people with just one copy. Those without any copies of the gene mutation are less likely to develop heart disease — even if they become obese. Natives of India and South Asia have a higher-than-average propensity for abdominal obesity. And white men and black women tend to accumulate more visceral fat than black men and white women.

Fat and aging

With age, people tend to lose muscle tissue, especially the type of specialized muscle fibers that produce quick bursts of speed and power. Fat frequently accumulates within the remaining muscle tissue, causing your body fat percentage to increase even when your weight remains constant. This scenario is closely linked to bodywide inflammation and diabetes risk. It may also explain why your BMI measurement doesn’t provide a true reflection of your health risks.

Evidence suggests that waist circumference and waist-to-hip ratio are better indicators of metabolic health than BMI. Even among people with the same BMI, those who have a large waist (defined as more than 40 inches for men and 35 inches for women) have a significantly higher risk. In addition, people who tend to carry their weight in their hips and thighs (a “pear” shape) have lower waist-to-hip ratios and are less prone to heart disease than people with abdominal obesity (an “apple” shape); see “Measuring your midsection.”

Measuring your midsection

To measure your waist accurately, exhale and wrap a measuring tape around your bare abdomen just above your navel (belly button). Don’t suck in your gut or pull the tape tight enough to squeeze the area.

To compute your waist-to-hip ratio, first measure your hips by putting the tape measure around the widest part of your buttocks. Keep the tape measure level. Then, divide your waist size by your hip size.

Measurements that signal high risk Waist (inches) Waist-to-hip ratio
Women 35 or more 0.9 or more
Men 40 or more 1.0 or more

What should you do about visceral fat?

People with abdominal obesity — even if they’re not overweight — can lessen their heart disease risk with regular exercise and healthy eating habits. “Reducing the total amount of fat in your body frees up storage space for fat particles in places that are associated with less metabolic risk,” says Dr. Mantzoros. That’s why losing as little as 7% of your total weight helps lower heart disease risk: the most dangerous visceral fat disappears first.

 

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Connie’s comments:
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  2. Do strength training
  3. Use music – toning relaxation music for brain health
  4. Eat colored whole food and get quality supplements at:

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Leptin and other pro inflammatory biomakers for chronic fatigue syndrome

Researchers identify biomarkers associated with chronic fatigue syndrome severity

Stanford investigators used high-throughput analysis to link inflammation to chronic fatigue syndrome, a difficult-to-diagnose disease with no known cure.

Man in a lab coat sitting near a microscope with a woman in a lab coat in the background

Jose Montoya and his colleagues have found evidence inflammation may be the culprit behind chronic fatigue syndrome, a disease with no known cure.
Steve Fisch

Researchers at the Stanford University School of Medicine have linked chronic fatigue syndrome to variations in 17 immune-system signaling proteins, or cytokines, whose concentrations in the blood correlate with the disease’s severity.

The findings provide evidence that inflammation is a powerful driver of this mysterious condition, whose underpinnings have eluded researchers for 35 years.

The findings, described in a study published online July 31 in the Proceedings of the National Academy of Sciences, could lead to further understanding of this condition and be used to improve the diagnosis and treatment of the disorder, which has been notably difficult.

More than 1 million people in the United States suffer from chronic fatigue syndrome, also known as myalgic encephomyelitis and designated by the acronym ME/CFS. It is a disease with no known cure or even reliably effective treatments. Three of every four ME/CFS patients are women, for reasons that are not understood. It characteristically arises in two major waves: among adolescents between the ages of 15 and 20, and in adults between 30 and 35. The condition typically persists for decades.

“Chronic fatigue syndrome can turn a life of productive activity into one of dependency and desolation,” said Jose Montoya, MD, professor of infectious diseases, who is the study’s lead author. Some spontaneous recoveries occur during the first year, he said, but rarely after the condition has persisted more than five years.

The study’s senior author is Mark Davis, PhD, professor of immunology and microbiology and director of Stanford’s Institute for Immunity, Transplantation and Infection.

‘Solid basis for a diagnostic blood test’

“There’s been a great deal of controversy and confusion surrounding ME/CFS — even whether it is an actual disease,” said Davis. “Our findings show clearly that it’s an inflammatory disease and provide a solid basis for a diagnostic blood test.”

Many, but not all, ME/CFS patients experience flulike symptoms common in inflammation-driven diseases, Montoya said. But because its symptoms are so diffuse —sometimes manifesting as heart problems, sometimes as mental impairment nicknamed “brain fog,” other times as indigestion, diarrhea, constipation, muscle pain, tender lymph nodes and so forth — it often goes undiagnosed, even among patients who’ve visited a half-dozen or more different specialists in an effort to determine what’s wrong with them.

Mark Davis

Mark Davis

Montoya, who oversees the Stanford ME/CFS Initiative, came across his first ME/CFS patient in 2004, an experience he said he’s never forgotten.

“I have seen the horrors of this disease, multiplied by hundreds of patients,” he said. “It’s been observed and talked about for 35 years now, sometimes with the onus of being described as a psychological condition. But chronic fatigue syndrome is by no means a figment of the imagination. This is real.”

Antivirals, anti-inflammatories and immune-modulating drugs have led to symptomatic improvement in some cases, Montoya said. But no single pathogenic agent that can be fingered as the ultimate ME/CFS trigger has yet been isolated, while previous efforts to identify immunological abnormalities behind the disease have met with conflicting and confusing results.

Still, the sporadic effectiveness of antiviral and anti-inflammatory drugs has spurred Montoya to undertake a systematic study to see if the inflammation that’s been a will-o’-the-wisp in those previous searches could be definitively pinned down.

To attack this problem, he called on Davis, who helped create the Human Immune Monitoring Center. Since its inception a decade ago, the center has served as an engine for large-scale, data-intensive immunological analysis of human blood and tissue samples. Directed by study co-author Holden Maecker, PhD, a professor of microbiology and immunology, the center is equipped to rapidly assess gene variations and activity levels, frequencies of numerous immune cell types, blood concentrations of scores of immune proteins, activation states of intercellular signaling models, and more on a massive scale.

Finding patterns

This approach is akin to being able to look for and find larger patterns — analogous to whole words or sentences — in order to locate a desired paragraph in a lengthy manuscript, rather than just try to locate it by counting the number of times in which the letter A appears in every paragraph.

The scientists analyzed blood samples from 192 of Montoya’s patients, as well as from 392 healthy control subjects. The average age of patients and controls was about 50. Patients’ average duration of symptoms was somewhat more than 10 years.

Importantly, the study design took into account patients’ disease severity and duration. The scientists found that some cytokine levels were lower in patients with mild forms of ME/CFS than in the control subjects, but elevated in ME/CFS patients with relatively severe manifestations. Averaging the results for patients versus controls with respect to these measures would have obscured this phenomenon, which Montoya said he thinks may reflect different genetic predispositions, among patients, to progress to mild versus severe disease.

I have seen the horrors of this disease, multiplied by hundreds of patients.

When comparing patients versus control subjects, the researchers found that only two of the 51 cytokines they measured were different. Tumor growth factor beta was higher and resistin was lower in ME/CFS patients. However, the investigators found that the concentrations of 17 of the cytokines tracked disease severity. Thirteen of those 17 cytokines are pro-inflammatory.

TGF-beta is often thought of as an anti-inflammatory rather than a pro-inflammatory cytokine. But it’s known to take on a pro-inflammatory character in some cases, including certain cancers. ME/CFS patients have a higher than normal incidence of lymphoma, and Montoya speculated that TGF-beta’s elevation in ME/CFS patients could turn out to be a link.

One of the cytokines whose levels corresponded to disease severity, leptin, is secreted by fat tissue. Best known as a satiety reporter that tells the brain when somebody’s stomach is full, leptin is also an active pro-inflammatory substance. Generally, leptin is more abundant in women’s blood than in men’s, which could throw light on why more women than men have ME/CFS.

More generally speaking, the study’s results hold implications for the design of future studies of disease, including clinical trials testing immunomodulatory drugs’ potential as ME/CFS therapies.

“For decades, the ‘case vs. healthy controls’ study design has served well to advance our understanding of many diseases,” Montoya said. “However, it’s possible that for certain pathologies in humans, analysis by disease severity or duration would be likely to provide further insights.”

Other Stanford co-authors of the study are clinical research coordinator Jill Anderson; Tyson Holmes, PhD, senior research engineer at the Institute for Immunity, Transplantation and Infection; Yael Rosenberg-Hasson, PhD, immunoassay and technical director at the institute; Cristina Tato, PhD, MPH, research and science analyst at the institute; former study coordinator Ian Valencia; and Lily Chu, MSHS, a board member of the Stanford University ME/CFS Initiative.

The study was funded by the National Institutes of Health (grant U19AI057229), the Stanford ME/CFS Initiative Fund and an anonymous donor.

Stanford’s departments of Medicine and of Microbiology and Immunology also supported the work.

Bruxism and proper root cause diagnosis – SLEEP APNEA?

BRUXISM AND PROPER ROOT CAUSE DIAGNOSIS – TMD OR SLEEP APNEA?

Are you screening for sleep apnea when treatment planning occlusal guards?

By Iman Sadri, DDS

There has been much buzz recently about the dentist’s role in the treatment of obstructive sleep apnea (OSA). Most of the attention has centered around oral appliance therapy as a treatment modality to replace the CPAP in the absence of severe OSA. Despite the increase in literature and a growing population affected by sleep apnea, too many dental professionals still drop the ball when making the right diagnosis for their patients. In many instances, when teeth grinding is charted during the clinical exam, dentists can be quick to diagnose an occlusal guard for their patients with bruxism. The focus immediately becomes on alleviating the symptoms as opposed to evaluating the cause. If teeth are worn down from potential grinding, an occlusal guard becomes the first and only treatment of choice, in many instances.

ADDITIONAL READING | Sleep apnea considerations for the restorative patient

When treatment planning for bruxism, many clinicians have been trained only to observe the 3 T’s: teeth, trauma, and TMJ. In some instances, treatment planning an occlusal guard when noting clenching or grinding may be a misdiagnosis. Bruxism, in some cases, can be a result of sleep apnea, as opposed to a symptom of TMD. In patients with OSA, teeth grinding can occur as a reactionary mechanism to wake the body during sleep when there is a lack of proper oxygen intake. A percentage of patients, including children, actually grind their teeth to wake themselves when the body is gasping for air during moments of apnea. Their bruxism may be a direct result of untreated sleep apnea.

ADDITIONAL READING | Hidden dental dangers of undiagnosed obstructive sleep apnea

Think about the last five occlusal guards that you delivered for your adult patients. Did you carefully examine the anatomy of the oral cavity, or did you simply evaluate the dentition? Did you consider other factors that could play a role in bruxism other than TMD? If the bruxism is a potential result from OSA, other pathologies in the oral cavity may include: scalloping of the tongue, elongated soft palate, large tonsils, enlarged uvula, retrognathia, severe overjet, narrow airway, enlarged neck size, and excessive skin and fat tissue around the neck and jawline. An elevated BMI and obesity are also common factors associated with OSA.

If patients feature some of the anatomical associations with OSA in addition to bruxism, then treating them with an occlusal guard may be the incorrect treatment modality. It is important to have patients at risk for OSA fill out an Epworth Sleepiness Scale form. A determination of their overall fatigue, energy level, snoring frequency, and daytime sleepiness can be assessed with the Epworth Sleepiness Scale. Following this assessment, if patients are at risk for having OSA, a polysomnograph (PSG) with a sleep technician should be scheduled. Only a physician such a pulmonologist or an ENT can actually diagnose obstructive sleep apnea from the results of the PSG. If a determination is made from the physician that the patient’s OSA can be alleviated with treatment other than CPAP, a custom-fitted oral appliance, such as a mandibular-positioning or a tongue-retaining device, could be considered for treatment with the proper assessment.

Dental professionals need to become properly trained in the field of sleep medicine to be more well versed with OSA. Understanding the physical manifestations that present with OSA in the oral cavity is imperative. In addition, becoming knowledgeable about the different types of oral appliances to treat OSA with or without CPAP is also necessary. Bruxism can be a byproduct of OSA, and some PSGs actually account for the number of bruxism episodes during a sleep cycle. Treatment planning an occlusal guard to treat the bruxism that is a result of OSA is not addressing the source of the pathology. If left untreated, sleep apnea can lead to significant health problems in patients. Some of the health risks associated with sleep apnea include type 2 diabetes and serious cardiovascular health ailments such as heart disease, stroke, heart attacks, and heart failure. It is estimated that 22 million Americans suffer from sleep apnea, and this statistic will only continue to rise with a growing population. Dentists must play their part in helping screen patients correctly for OSA. If patients present with bruxism, an occlusal guard may not be the only treatment solution. So, the next time you ask your patients if they grind their teeth, also ask them if they snore.

Iman Sadri, DDS Iman Sadri, DDS, is a cosmetic dentist and writer. He is a 2008 graduate of the NYU College of Dentistry and maintains a private practice in Orange County, Calif. 

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