Author: Rob

Dietary intervention restores protective protein and decreases death rate in mice

Source: Society for Neuroscience

The incidence of dementia and Alzheimer’s continues to escalate in the general population.

LCHF/Keto diets have proven to be beneficial to individuals dealing with these health issues.

It has been suggested that these conditions may partly be due to impaired glucose metabolism in the brain, hence the increasing use of the term “Type 3 Diabetes”.

Enabling the brain to use ketones for its energy source therefore can provide some benefit with regards to brain function.

A major challenge with this is that a radical dietary shift in the geriatric population can be quite challenging – if not impossible.

Usage of exogenous ketone compounds is one potential option in this situation.

Following is an article from Science Daily which talks about published research which suggests that increasing ketone levels in the diet can help to protect neurons from death during the progression of Alzheimer’s disease.

Summary: A ketone-supplemented diet may protect neurons from death during the progression of Alzheimer’s disease, according to research in mice.

A ketone-supplemented diet may protect neurons from death during the progression of Alzheimer’s disease, according to research in mice recently published in JNeurosci.

Early in the development of Alzheimer’s disease, the brain becomes over excited, potentially through the loss of inhibitory, or GABAergic, interneurons that keep other neurons from signaling too much. Because interneurons require more energy compared to other neurons, they may be more susceptible to dying when they encounter the Alzheimer’s disease protein amyloid beta. Amyloid beta has been shown to damage mitochondria — the metabolic engine for cells — by interfering with SIRT3, a protein that preserves mitochondrial functions and protects neurons.

Cheng et al. genetically reduced levels of SIRT3 in mouse models of Alzheimer’s disease. Mice with low levels of SIRT3 experienced a much higher mortality rate, more violent seizures, and increased interneuron death compared to the mice from the standard Alzheimer’s disease model and control mice. However, the mice with reduced levels of SIRT3 experienced fewer seizures and were less likely to die when they ate a diet rich in ketones, a specific type of fatty acid. The diet also increased levels of SIRT3 in the mice.

Increasing SIRT3 levels via ketone consumption may be a way to protect interneurons and delay the progression of Alzheimer’s disease.


Story Source:

Materials provided by Society for Neuroscience. Note: Content may be edited for style and length.


Journal Reference:

  1. Aiwu Cheng, Jing Wang, Nathaniel Ghena, Qijin Zhao, Isabella Perone, M. Todd King, Richard L. Veech, Myriam Gorospe, Ruiqian Wan, Mark P. Mattson. SIRT3 Haploinsufficiency Aggravates Loss of GABAergic Interneurons and Neuronal Network Hyperexcitability in an Alzheimer’s Disease Model. The Journal of Neuroscience, 2019; 1446-19 DOI: 10.1523/JNEUROSCI.1446-19.2019

Abstract

SIRT3 Haploinsufficiency Aggravates Loss of GABAergic Interneurons and Neuronal Network Hyperexcitability in an Alzheimer’s Disease Model

Impaired mitochondrial function and aberrant neuronal network activity are believed to be early events in the pathogenesis of Alzheimer’s disease (AD), but how mitochondrial alterations contribute to aberrant activity in neuronal circuits is unknown. In this study, we examined the function of mitochondrial protein deacetylase sirtuin 3 (SIRT3) in the pathogenesis of AD. Compared to AppPs1 mice, Sirt3-haploinsufficient AppPs1 mice (Sirt3+/-AppPs1) exhibit early epileptiform EEG activity and Seizure. Both male and female Sirt3+/-AppPs1 mice were observed to die prematurely before five months of age.

When comparing male mice among different genotypes, Sirt3 haploinsufficiency renders GABAergic interneurons in the cerebral cortex vulnerable to degeneration and associated neuronal network hyperexcitability. Feeding Sirt3+/-AppPs1 AD mice with a ketone ester-rich diet increases SIRT3 expression and prevents seizure-related death and the degeneration of GABAergic neurons, indicating that the aggravated GABAergic neuron loss and neuronal network hyperexcitability in Sirt3+/-AppPs1 mice are caused by SIRT3 reduction and can be rescued by increase of SIRT3 expression. Consistent with a protective role in AD, SIRT3 levels are reduced in association with cerebral cortical Aβ pathology in AD patients. In summary, SIRT3 preserves GABAergic interneurons and protects cerebral circuits against hyperexcitability, and this neuroprotective mechanism can be bolstered by dietary ketone esters.

SIGNIFICANCE STATEMENT

GABAergic neurons provide the main inhibitory control of neuronal activity in the brain. By preserving mitochondrial function, SIRT3 protects parvalbumin and calretinin interneurons against Aβ-associated dysfunction and degeneration in AppPs1 AD mice, thus restraining neuronal network hyperactivity. The neuronal network dysfunction that occurs in AD can be partially reversed by physiological, dietary, and pharmacological interventions to increase SIRT3 expression and enhance the functionality of GABAergic interneurons.
 

Fasting in its many forms can provide profound beneficial health benefits.

Following is an article on this topic authored by Dr. Dan Pompa which provides a good overview.

Regards,

Robert (Rob) Lamberton

Fasting is a very old ritual to boost health that is found in religions all over the world and is rooted in natural ancestral cycles of feast and famine. Before we had grocery stores, restaurants, and even food delivery services- there were often times with very little to no food. Following times of famine,  there was an abundance of food (following a successful harvest, forage, or hunt). Even animal wisdom harnesses the power of fasting- like dogs, that will intuitively stop eating when they are sick. More and more studies are emerging on the incredible benefits that fasting can have, on not only for health but also suggesting a boost in longevity.

Fasting diets have nothing to do with WHAT or HOW MUCH you eat, but WHEN you eat. Intermittent fasting (or IF) is the art of restricted time eating, so instead of counting calories or restricting what types of foods you eat- the entire “diet” relies on when you do, and don’t eat.

Recent Research on Fasting

Have Your Cake And Eat It Too: Boost Health and Longevity Not By Changing What You Eat, But When You Eat.

Intermittent Fasting Research

Although Intermittent Fasting to boost health has gained popularity in more recent years, its wisdom dates back to our ancestors from the stone age. Apart from periods of feast and famine, our ancestors’ lives were also heavily dictated by the rising and setting of the sun; activities like eating naturally happened during day time. Our exposure to light, food, and movement are the main tenets that inform and program our circadian rhythm. This internal rhythm influences everything from sleep-wake cycles, hormone release, eating habits and digestion, body temperature, and other important bodily functions.1 Intermittent fasting plays a role in giving the body an adequate period of rest from digestion, enabling it to not only heal- but thrive.

Research on Fasting is Extensive

Many of the studies regarding fasting to boost health and longevity have been done on animals. However, these studies suggest promising effects on metabolic functions, health, and lifespan for humans. Although there are many variables, Rafael deCabo, a scientist at the National Institute on Aging and the study’s lead author explains that;

“in the absence of calorie restriction, and independent of diet composition, fasting mice do better than non-fasting”.2

Boost Health! The ever-increasing research regarding fasting suggests some incredible health and longevity benefits including:

  • Autophagy
  • A boost in stem cells
  • Boost in ketones
  • Hormone optimization
  • Increased insulin sensitivity
  • Reset of the microbiome
  • Reset of the DNA (gene code)
  • Decrease in inflammation
  • A decrease in oxidative stress
  • Reduced instances of chronic disease and obesity
  • Protection against unusual deterioration of cognitive function
  • Fat loss
  • Cancer prevention
  • Promotion of better sleep
  • More satiety/ reduced hunger

Although benefits are often examined as individual points, they are in fact very much intertwined to promote overall longevity. One of the main ways IF leads to longevity is “multi-system regeneration,” which fasting researcher Dr. Valter Longo explains occurs during the presence of ketones in the blood. The autophagy process that happens during a fasting period breaks down weak and damaged cells, which are then replaced with new stem cells after food is reintroduced.

“You get rid of the junk during starvation — and once you have food, you can rebuild… The damaged cells are replaced with new cells, working cells — and now the system starts working properly.”

Research on Fasting: Health and Longevity

All these benefits suggest a direct link between fasting and longevity, although conducting a clinical longevity study in humans is unfeasible at the moment, for would cost “a hundred million dollars or more,” according to Longo. “But if you look at the data from our trial … it would be hard to see how they would not live longer.”

Dr. Valter Longo and Dr. Satchin Panda’s study demonstrated that a 12-hour feeding window reduced blood cholesterol, fasting blood sugar, body weight, body fat, inflammation, and dysbiosis, and increased energy expenditure, motor control, endurance, sleep, and cardiac function.3 Their study examined the intricate relationship between time-restricted feeding (IF), circadian health, and ultimately concluded that simply limiting your eating window to a minimum of 12 hours reduces biological age irrelevant of any dietary changes! Indeed, their study suggests that you can have your cake and eat it too… so long as you do so within your eating window.

Research on Fasting: How To Do It

There are many different fasting styles that range from multiple days water-only fasts, to bone broth fasts, to alternate day fasting… but intermittent fasting itself is conceptually incredibly simple: engage in a particular restricted eating window, preferably rooted in 2 meals (and no snacking). This might seem not too far off from your current habits, but studies show the average American eats 17-21 times a day! This is detrimental to our health and longevity.

Classic Intermittent Fasting: The Eating Window

The key is, aforementioned, restricting your eating window. The science suggests a very minimum of 12 hours to see any benefits, so if you have no experience fasting- start there. If you eat your first meal at 8 am, no food (or beverage other than plain water) after 8 pm.4 From there, extend the fasting window to ideally (at least) 16 hours. Whether you decide to skip breakfast or dinner is completely personal, find what works best for your schedule and which option is more sustainable over the long run. A 2018 study comparing a 12-hour feeding window to an 8-hour feeding window demonstrated that although both groups lost weight, those in the 8-hour feeding window group dramatically lower insulin levels, improved insulin sensitivity, and significantly lower blood pressure in only five weeks.5

Research on Fasting: One Meal a Day

“One meal a day” (or OMAD) is an extreme version of intermittent fasting. An individual shortens their eating window to essentially the duration of one single meal. The benefits of this technique essentially amplify all the aforementioned benefits of a 16/8 IF protocol.  OMAD gives the body even more time in this resting (vs. digesting) state. OMAD is not, however, for everyone- nor should it be the goal. Consuming one meal a day can be more taxing on the adrenal system. OMAD could even induce more detoxification than an individual can handle at once.

Like any type of good stress (exercise, sauna, cold therapy), the adrenals and overall system need to be strong enough to withstand the short term stressor. Ease into intermittent fasting at your own pace, and always listen to your body. A great way to transition into it and/ or reboot your system is to take part in the 5-day Fasting Mimicking Diet™.

Research on Fasting to Boost Health and Longevity: The Fasting Mimicking DietTM

Fasting for health and longevity can be a daunting endeavor for someone who is used to eating 3+ meals a day their entire lives, and this is where the fasting mimicking diet comes in. Fasting expert and researcher Dr. Valter Longo created the Fasting Mimicking Diet program that mimics the benefits of a fasting protocol, combining both the benefits of intermittent fasting and a longer term fast (through caloric restriction). Prolon® takes out the guesswork but providing clients with all their meals for a 5 day period. Longo is the Director of both the Longevity Institute at the University of Southern California and The Program on Longevity and Cancer at IFOM in Milan, and his clinical study demonstrated remarkable benefits that fasting has to offer in just 5 days (repeated for 3 months):

Promote stem cell-based renewal in the body

Decrease excess body fat while preserving lean muscle mass

Maintain healthy levels of blood glucose, cholesterol, & blood pressure

Decreased hormone IGF-1 (which has been implicated with aging and disease)6

We suggest using this fasting mimicking diet to boost health if you are completely new to fasting or are trying to break destructive eating patterns! This can be a bridge to continue on with regular Intermittent Fasting thereafter!

References

  1. Longo, Valter D., and Satchidananda Panda. “Fasting, Circadian Rhythms, and Time-Restricted Feeding in Healthy Lifespan.” Cell Metabolism, vol. 23, no. 6, 2016, pp. 1048–1059., doi:10.1016/j.cmet.2016.06.001.
  2. Mitchell, Sarah J., et al. “Daily Fasting Improves Health and Survival in Male Mice Independent of Diet Composition and Calories.” Cell Metabolism, vol. 29, no. 1, Jan. 2019, doi:10.1016/j.cmet.2018.08.011
  3. NIH. “Circadian Rhythms.” National Institute of General Medical Sciences, U.S. Department of Health and Human Services, 2017, www.nigms.nih.gov/Education/Pages/Factsheet_CircadianRhythms.aspx
  4. Sutton, Elizabeth F., et al. “Early Time-Restricted Feeding Improves Insulin Sensitivity, Blood Pressure, and Oxidative Stress Even without Weight Loss in Men with Prediabetes.” Cell Metabolism, vol. 27, no. 6, 2018, doi:10.1016/j.cmet.2018.04.010.
  5. Wei, Min, et al. “Fasting-Mimicking Diet and Markers/Risk Factors for Aging, Diabetes, Cancer, and Cardiovascular Disease.” Science Translational Medicine, vol. 9, no. 377, 2017, doi:10.1126/scitranslmed.aai8700.

Here is a great article from the Science Alert website which discusses what the consumption of sugar does to the brain.

We love sweet treats. But too much sugar in our diets can lead to weight gain and obesity, Type 2 diabetes and dental decay. We know we shouldn’t be eating candy, ice cream, cookies, cakes and drinking sugary sodas, but sometimes they are so hard to resist.

It’s as if our brain is hardwired to want these foods.

As a neuroscientist my research centres on how modern day “obesogenic”, or obesity-promoting, diets change the brain. I want to understand how what we eat alters our behaviour and whether brain changes can be mitigated by other lifestyle factors.

Your body runs on sugar – glucose to be precise. Glucose comes from the Greek word glukos which means sweet. Glucose fuels the cells that make up our body – including brain cells (neurons).

Dopamine “hits” from eating sugar

On an evolutionary basis, our primitive ancestors were scavengers. Sugary foods are excellent sources of energy, so we have evolved to find sweet foods particularly pleasurable. Foods with unpleasant, bitter and sour tastes can be unripe, poisonous or rotting – causing sickness.

So to maximize our survival as a species, we have an innate brain system that makes us like sweet foods since they’re a great source of energy to fuel our bodies.

When we eat sweet foods the brain’s reward system – called the mesolimbic dopamine system – gets activated. Dopamine is a brain chemical released by neurons and can signal that an event was positive. When the reward system fires, it reinforces behaviours – making it more likely for us to carry out these actions again.

Dopamine “hits” from eating sugar promote rapid learning to preferentially find more of these foods.

Our environment today is abundant with sweet, energy rich foods. We no longer have to forage for these special sugary foods – they are available everywhere.

Unfortunately, our brain is still functionally very similar to our ancestors, and it really likes sugar. So what happens in the brain when we excessively consume sugar?

Can sugar rewire the brain?

The brain continuously remodels and rewires itself through a process called neuroplasticity. This rewiring can happen in the reward system. Repeated activation of the reward pathway by drugs or by eating lots of sugary foods causes the brain to adapt to frequent stimulation, leading to a sort of tolerance.

In the case of sweet foods, this means we need to eat more to get the same rewarding feeling – a classic feature of addiction.

Food addiction is a controversial subject among scientists and clinicians. While it is true that you can become physically dependent on certain drugs, it is debated whether you can be addicted to food when you need it for basic survival.

The brain wants sugar, then more sugar

Regardless of our need for food to power our bodies, many people experience food cravings, particularly when stressed, hungry or just faced with an alluring display of cakes in a coffee shop.

To resist cravings, we need to inhibit our natural response to indulge in these tasty foods. A network of inhibitory neurons is critical for controlling behaviour. These neurons are concentrated in the prefrontal cortex – a key area of the brain involved in decision-making, impulse control and delaying gratification.

Inhibitory neurons are like the brain’s brakes and release the chemical GABA. Research in rats has shown that eating high-sugar diets can alter the inhibitory neurons. The sugar-fed rats were also less able to control their behaviour and make decisions.

Importantly, this shows that what we eat can influence our ability to resist temptations and may underlie why diet changes are so difficult for people.

A recent study asked people to rate how much they wanted to eat high-calorie snack foods when they were feeling hungry versus when they had recently eaten. The people who regularly ate a high-fat, high-sugar diet rated their cravings for snack foods higher even when they weren’t hungry.

This suggests that regularly eating high-sugar foods could amplify cravings – creating a vicious circle of wanting more and more of these foods.

Sugar can disrupt memory formation

Another brain area affected by high sugar diets is the hippocampus – a key memory centre.

Research shows that rats eating high-sugar diets were less able to remember whether they had previously seen objects in specific locations before.

The sugar-induced changes in the hippocampus were both a reduction of newborn neurons, which are vital for encoding memories, and an increase in chemicals linked to inflammation.

How to protect your brain from sugar?

The World Health Organization advises that we limit our intake of added sugars to five per cent of our daily calorie intake, which is 25 grams (six teaspoons).

Considering the average Canadian adult consumes 85 grams (20 teaspoons) of sugar per day, this is a big diet change for many.

Importantly, the brain’s neuroplasticity capabilities allow it to reset to an extent following cutting down on dietary sugar, and physical exercise can augment this process. Foods rich in omaga-3 fats (found in fish oil, nuts and seeds) are also neuroprotective and can boost brain chemicals needed to form new neurons.

While it’s not easy to break habits like always eating dessert or making your coffee a double-double, your brain will thank you for making positive steps.

The first step is often the hardest. These diet changes can often get easier along the way.

Amy Reichelt, BrainsCAN Research Associate, Western University.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Both the U.S. and Canadian governments have been reluctant to include the LCHF (low carb, high fat)/Keto diet as an acceptable option for the populations in both countries.

We recently experienced this here in Canada when the Canadian government revised the Canada food guidelines and despite a significant lobbying effort by researchers, clinicians and the general public they chose to not include the LCHF/Keto diet.

Now in the U.S. a coalition of stakeholders has formed to lobby the U.S. government to include the LCHF/Keto diet in its recommendations.

This group of stakeholders includes researchers, clinicians and members of the general public.

It is only a matter of time before both governments incorporate the LCHF/Keto diet into their recommendations.

There is no one diet that works for everyone but there is no denying the considerable research that has been published on the health benefits of the LCHF/Keto diets, including weight management, potential reversal of Type 2 Diabetes, dementia and Alzheimer’s and many more.

Here is an article from the Natural Practitioner magazine on this topic.

A new group called the Low-Carb Action Network (LCAN), a coalition of doctors, academics, and average Americans with personal success stories using low-carb diets, has launched to urge U.S. nutrition leaders to include a true low-carb diet as part of the 2020 Dietary Guidelines for Americans (DGA).

LCAN members point to a large and rapidly growing body of strong scientific research showing carbohydrate restriction to be a safe and effective strategy to prevent and even reverse chronic, diet-related conditions such as pre-diabetes/type 2 diabetes, overweight/obesity and high blood pressure along with a broad array of other cardiovascular risk factors.

The American Diabetes Association (ADA) recently endorsed low-carb/keto diets as a standard of care for the prevention and management of type 2 diabetes, stating that the diet lowers blood pressure, controls blood sugar, lowers triglycerides (fatty acids in the blood), raises the “good” cholesterol (HDL-C), and reduces the need for medication use.

However, the DGA does not include a low-carb diet. For the 2015 DGA, USDA-HHS ignored some 70 clinical trials demonstrating the effectiveness of low-carb diets. LCAN does not want important scientific evidence to again be ignored.

LCAN members are also concerned that USDA (U.S. Department of Agriculture), in its current scientific reviews, is using an inaccurate definition of the diet that is not up-to-date with current science and will lead to misleading, untrustworthy results. Specifically, USDA is defining “low-carb” as 45 percent of total calories or less, when leaders in the field agree this number should be 25 percent.

Dr. Eric Westman, associate professor of medicine at Duke University emphasized that the current dietary guidelines do not apply to most Americans and that a variety of dietary options should be presented to the American people, including a low-carbohydrate diet.“One size does not fit all. If there is anything we’ve learned over the last four years, it’s that the low-carb approach should be a viable option,” he stated.

Dr. Mark Cucuzzella, professor of Family Medicine at West Virginia University added that a a majority of the patients he treats daily have obesity and “metabolic syndrome,” a combination of conditions driven by hyperinsulinemia that increase the risk of heart disease, stroke and diabetes.

“If the government has any responsibility to give advice on nutrition it should be focused on those who have a medical condition which is impacted by nutrition and provide evidence-based nutrition solutions, one being a low-carb diet. This diet is highly effective to prevent and treat diet-related illnesses and has decades of evidence to support it.

A study conducted last year by the University of North Carolina at Chapel concluded that only 12 percent of American adults are metabolically healthy, while 88 percent are on the way to developing type 2 diabetes, cardiovascular disease or another chronic, diet-related condition.

Dr. Nadir Ali, chairman, department of cardiology, Clear Lake Regional Medical Center, and research professor, Department of Nutrition and Applied Science, University of Houston in Texas, has significant experience in the science and practice of low-carb diets.

“As a cardiologist, I regularly prescribe a low-carb diet to treat patients with type 2 diabetes and other heart-related diseases to better their health and improve their quality of life,” said Dr. Ali. “Given the significant amount of scientific research and evidence supporting this diet, it’s time for U.S. nutrition policy leaders to prescribe a low-carb option for those who are tipping into obesity, diabetes, high blood pressure and more.”

LCAN plans to launch a grassroots campaign in the coming months to urge leaders at USDA and HHS to ensure that a properly defined low-carb diet is included in the DGA to provide a dietary option for the majority of Americans who suffer from diet-related, chronic diseases. The next meeting of the Dietary Guidelines Advisory Committee will be held next month in Houston.

For more information, visit https://lowcarbaction.org.

Dietary intervention restores protective protein and decreases death rate in mice

Date: December 9, 2019
Source: Society for Neuroscience Summary:

A ketone-supplemented diet may protect neurons from death during the progression of Alzheimer’s disease, according to research in mice.

I am a big proponent of LCHF (low carb, high fat)/ketogenic diets – this diet has worked well for myself and I have seen it provide many significant benefits in clients I work with.

No one diet will work for everyone however LCHF diets can be extremely beneficial – if not followed continuously then periodically almost like one would do a detox program.

Following is an article which appeared in Science Daily based upon a study published in the Journal of Neuroscience.

This study suggests that consumption of ketones may be protective against the progression of Alzheimer’s.

A ketone-supplemented diet may protect neurons from death during the progression of Alzheimer’s disease, according to research in mice recently published in JNeurosci.

Early in the development of Alzheimer’s disease, the brain becomes over excited, potentially through the loss of inhibitory, or GABAergic, interneurons that keep other neurons from signaling too much. Because interneurons require more energy compared to other neurons, they may be more susceptible to dying when they encounter the Alzheimer’s disease protein amyloid beta. Amyloid beta has been shown to damage mitochondria — the metabolic engine for cells — by interfering with SIRT3, a protein that preserves mitochondrial functions and protects neurons.

Cheng et al. genetically reduced levels of SIRT3 in mouse models of Alzheimer’s disease. Mice with low levels of SIRT3 experienced a much higher mortality rate, more violent seizures, and increased interneuron death compared to the mice from the standard Alzheimer’s disease model and control mice. However, the mice with reduced levels of SIRT3 experienced fewer seizures and were less likely to die when they ate a diet rich in ketones, a specific type of fatty acid. The diet also increased levels of SIRT3 in the mice.

Increasing SIRT3 levels via ketone consumption may be a way to protect interneurons and delay the progression of Alzheimer’s disease.


Story Source:

Materials provided by Society for Neuroscience. Note: Content may be edited for style and length.


Journal Reference:

  1. Aiwu Cheng, Jing Wang, Nathaniel Ghena, Qijin Zhao, Isabella Perone, M. Todd King, Richard L. Veech, Myriam Gorospe, Ruiqian Wan, Mark P. Mattson. SIRT3 Haploinsufficiency Aggravates Loss of GABAergic Interneurons and Neuronal Network Hyperexcitability in an Alzheimer’s Disease Model. The Journal of Neuroscience, 2019; 1446-19 DOI: 10.1523/JNEUROSCI.1446-19.2019

One of the major issues causing problems with losing weight and maintaining a healthy weight is due to the presence of chemicals in the body – environmental toxins.

Some of these chemicals are called “obesogens” – because they cause obesity and it is almost impossible for an individual to lose weight until these compounds are removed.

A key compound in this category is phthalates, often referred to as plasticizers.

Weight issues for individuals have reached epidemic proportions across the world – in the U.S. alone, 39.8% of adults aged 20 and over are obese.

Historically, the suggested solution to this significant issue was to eat less and exercise more – in fact this is the advice that most MDs will currently suggest to their patients who are struggling with weight issues.

Losing weight and maintaining a healthy weight is certainly not as simple as eating less and exercising more, although these factors can provide benefits.

Other factors may include, and this is certainly not an exhaustive list the following – hormonal imbalance, including elevated cortisol levels, inflammation, genetic mutations, a diet which includes poor quality food sources, lack of sleep, stress and many more.

The way to rid the body of these chemicals is through a supervised detox program.

This should be done under the supervision of a health care practitioner knowledgeable in this area as freeing up these chemicals can cause significant problems if the body has not been prepared properly to excrete these chemicals.

Following is an article published by Functional Medicine University which discusses this topic.

Difficulty Losing Fat? This May Be the Cause

Ronald Grisanti D.C., D.A.B.C.O., DACBN, MS, CFMP

Obesity has hit epidemic proportions and the world is desperate to do anything to lose their unwanted fat.

Although eating a healthy diet and exercise is paramount to losing fat, there is one little unknown fact that will prevent millions of people from ever losing fat.

According to the US government this one thing is the considered the number one pollutant in the human body and will put a quick halt to ever reaching your desired level of fitness and fat loss.

One of the major causes of the obesity epidemic is the unprecedented level of phthalates or plasticizers.

The problem with these toxic environmental toxins is the fact that they are difficult to impossible to avoid. In fact they are found in every species even in the most pristine wild.

In fact we have so damaged the chemistry of even animals in the wild that the polar bears in the Arctic have human diseases such as hypothyroidism and osteoporosis.

Phthalates are the highest pollutant in the body being over 10,000 times higher than any of the thousands of other environmental toxins.

In fact they are so pervasive that now children six years of age have levels that used to take adults until the age of 40 to accumulate.

Phthalates are the highest pollutant in the body being over 10,000 times higher than any of the thousands of other environmental toxins.

Phthalates are the highest pollutant in the body being over 10,000 times higher than any of the thousands of other environmental toxins.

The government agencies, scientific and medical literature have clearly documented that a huge amount of these environment toxins (phthalates) come from our water, soda and infant formula bottles, food packaging, cosmetics, nail polish, mattresses, couches, carpets, clothing, medications, styrofoam cups, IVs, vinyl flooring, construction materials, home wiring, computers, industrial and auto exhausts, etc.,

The sad point is the fact that these toxins stockpile in the body and overwhelm our ability to detoxify them.

We routinely measure them with a wonderful test called Phthalates & Parabens Profile (https://www.gdx.net/product/phthalates-parabens-test-urine)

In addition to the damage these environmental toxins do to the biochemistry of losing fat they have also been known to be associated with difficult to treat chronic fatigue syndrome,fibromyalgia, ADD,  syndrome X, diabetes, arteriosclerosis, allergies, and much more.

In fact the label that a disease has is now unimportant. All we care about is what caused the disease and what biochemical corrections are necessary to get rid of it and actually bring about a true solution, a word you rarely hear in drug-oriented medicine.

What is even worse is the fact a pregnant mother’s phthalate levels (look at how many are continually drinking from plastic water bottles, etc., thinking that it’s something healthful) hugely influence not only the development of the child’s brain and glands, but even future fertility and cancers in their unborn children, not to mention, of course, obesity.

What you need to understand and something the researchers have forgot to mention is the fact that fat stores a huge amount of our chemicals, so the fatter you are the more the difficult it is to lose fat. Interesting and at the same time depressing.

The bottom line is many people will never lose weight or solve their medical problems because they have not gotten rid of the phthalates and other environmental pollutants that have damaged their chemistry and genetics.

One of the key ingredients to ridding the body of these harmful toxins is first to do what you can to avoid it (STOP DRINKING OUT OF STYROFORM CUPS and PLASTIC BOTTLES) and invest in a far infrared sauna

References:

Heindal JJ, Endocrine disruptors and the obesity epidemic, Toxicol Sci 76; 2:247-49, 2003

Baillie-Hamilton PF, Chemical toxins: a hypothesis to explain the global obesity epidemic, JAIt Complement Med 8;2:185-92, 2002

Alonso-Magdalena P, et al, The estrogenic effect of bisphenol A disrupts pancreatic B-cell function in vivo and induces insulin resistance, Environ Health Perspect 114:106-12, 2006

The Hundred Year Diet in the Wall Street (May 10, 2010, A I5)

Vom Saal FS, Welshons WV, Large effects from small exposures. II. The importance of positive controls in low-dose research on bisphenol A, Environ Res, 100;1:50-76, Jan. 2006

Feige JN, et al, The endocrine disruptor monoethyl-hexyl phthalate is a selective peroxisome proliferator-activated receptor gamma modulator that promotes adipogenesis, JBiol Chem 282:19152-66, 2007

Hatch EE, et al., Association of urinary phthalate metabolite concentrations with a body mass index and waist circumference: a cross-sectional study of NHANES data, 1999-2002, Environ Health 7:27, 2008

Clark K, et al, Observed concentrations in the environment. In: The Handbook of Environmental Chemistry. Vol 3, Part Q. Phthalate Ester (Staples CA, ed). New York: Springer, 125-177, 2003

Feige JN, et al, The pollutant diethylhexyl phthalate regulates hepatic energy metabolism via species-specific PPARa-dependent mechanisms, Environ Health Persp, 118; 2:234-41, Feb 2010

Jaakkola JJK, et al, The role of exposure to phthalates from polyvinyl chloride products in the development of asthma and allergies: A systematic review and meta-analysis, Environ Health Perspect 116:845-53, 2008