Maternal Obesity, Diabetes Associated With Autism, Other Developmental Disorders

A major study has found strong links between maternal diabetes and obesity and the likelihood of having a child with autism spectrum disorder (ASD) or another developmental disorder. (Credit: © kavring / Fotolia)

Wow this is a very alarming article from Science Daily: with the prevalence of obesity in North America and in other countries, we are headed for an explosion in the future of the prevalence of kids with autism spectrum disorder (ASD).

All the more reason to ensure that your leptin is in balance…

Regards,

Rob

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ScienceDaily (Apr. 9, 2012) — A major study conducted by researchers affiliated with the UC Davis MIND Institute has found strong links between maternal diabetes and obesity and the likelihood of having a child with autism spectrum disorder (ASD) or another developmental disorder.


The study, which investigated the relationships between maternal metabolic conditions and the risk of neurodevelopmental disorders, found that mothers who were obese were 67 percent more likely to have a child with ASD than normal-weight mothers without diabetes or hypertension, and were more than twice as likely to have a child with another developmental disorder.

Mothers with diabetes were found to have nearly 67 percent more likely to have a child with developmental delays as healthy mothers. However, the proportion of mothers with diabetes who had a child with ASD was higher than in healthy moms but did not reach statistical significance.

The study also found that the children of diabetic mothers who had ASD were more disabled — had greater deficits in language comprehension and production and adaptive communication — than were the children with ASD born to healthy mothers.

However, even children without ASD born to diabetic mothers exhibited impairments in socialization in addition to language comprehension and production, when compared with the non-ASD children of healthy women. Children without ASD of mothers with any of the metabolic conditions displayed mild deficits in problem solving, language comprehension and production, motor skills and socialization.

“Over a third of U.S. women in their childbearing years are obese, and nearly one-tenth have gestational or type 2 diabetes during pregnancy. Our finding that these maternal conditions may be linked with neurodevelopmental problems in children raises concerns and therefore may have serious public-health implications,” said Paula Krakowiak, a PhD Candidate in Epidemiology affiliated with the MIND Institute. “And while the study does not conclude that diabetes and obesity cause ASD and developmental delays, it suggests that fetal exposure to elevated glucose and maternal inflammation levels adversely affect fetal development.”

The study, “Maternal metabolic conditions and risk for autism and other neurodevelopmental disorders,” is published online April 9 in Pediatrics, the Journal of the American Academy of Pediatrics. Its authors said that it is the first study to examine the associations between neurodevelopmental disorders and maternal metabolic conditions not restricted solely to type 2 or gestational diabetes. It is also the first to include obesity and hypertension, which have similar underlying biological characteristics, and to investigate correlations between these conditions and impairments in the skills and abilities of children in specific developmental domains.

Over 60 percent of U.S. women of childbearing age are overweight; 34 percent are obese; and 16 percent have metabolic syndrome. Nearly 9 percent of U.S. women of childbearing age are diabetic, and more than 1 percent of U.S. pregnancies were complicated by chronic hypertension. In California, where the study was conducted, 1.3 percent of women had type 2 diabetes, and 7.4 percent had gestational diabetes.

Autism spectrum disorder is characterized by impairments in social interaction, communication deficits and repetitive behaviors and often is accompanied by intellectual disability. An estimated 1 in 88 children born today will be diagnosed with autism spectrum disorder, according to statistics recently released by the U.S. Centers for Disease Control and Prevention. An estimated 1 in 83 U.S. children has another developmental disorder, which includes other disorders resulting in intellectual disability.

The study included 1,004 mother/child pairs from diverse backgrounds enrolled in the Childhood Autism Risks from Genetics and the Environment Study (CHARGE), most of them living in Northern California, with a small subset living in Los Angeles. The children were between 24 and 60 months old, born in California and resided with at least one biological parent who spoke either English or Spanish. There were 517 children who had ASD; 172 who had other developmental disorders but not ASD; and 315 who were developing typically. The participants were enrolled between January 2003 and June 2010.

The researchers obtained demographic and medical information for the mothers and their children using the CHARGE Study Environmental Exposure Questionnaire, a telephone survey, the study participants’ birth files and medical records. The primary metabolic conditions of interest were type 2 diabetes or gestational diabetes.

Women were considered diabetic if the condition was noted in their medical records or if during the telephone surveys they answered “yes” to the questions “During this pregnancy were you ever told by a physician or nurse that you had gestational diabetes?” or “At any time before you became pregnant were you told by a doctor that you had [type 2] diabetes?” The same wording was used to obtain information about hypertension. BMI was calculated using height and weight prior to pregnancy from medical records or telephone interviews.

To confirm the developmental diagnoses of the children with ASD researchers used the Autism Diagnostic Interview-Revised (ADIR) and the Autism Diagnostic Observation Schedules (ADOS). All of the children were administered the Mullen Sales of Early Learning and the Vineland Adaptive Behavior Scales to assess their cognitive and adaptive development. Spanish-speaking children were administered the tests in Spanish. The participants were then divided into groups of children with ASD, developmental delay or typical development.

Among children whose mothers were diabetic during their pregnancies, the study found that the percentage of children with ASD born to women with type 2 diabetes or gestational diabetes (9.3 percent) or developmental disability (11.6 percent) was higher than the 6.4 percent of children with ASD born to women without these metabolic conditions.

Over 20 percent of the mothers of children with ASD or developmental delay were obese, compared with 14 percent of the mothers of typically developing children.

Approximately 29 percent of the children with ASD had mothers with a metabolic condition, and nearly 35 percent of the children with developmental delay had mothers with metabolic conditions. In contrast, 19 percent of the typically developing children had mothers with a metabolic condition.

The study also examined the link between hypertension and ASD or developmental disorders. The prevalence of high blood pressure was low for all groups, but more than two times higher among mothers of children with ASD or developmental delay than among mothers of children with typical development, though the finding did not reach statistical significance.

Analyses of the children’s cognitive abilities found that, among the children with ASD, children of mothers with diabetes exhibited poorer performance on tests of expressive and receptive language and communication skills of everyday living when compared with the children of healthy mothers. And the presence of any metabolic condition was associated with lower scores on all of the tests among children without ASD.

The authors note that obesity is a significant risk factor for diabetes and hypertension, and is characterized by increased insulin resistance and chronic inflammation, as are diabetes and hypertension. In diabetic, and possibility pre-diabetic pregnancies, poorly regulated maternal glucose can result in prolonged fetal exposure to elevated maternal glucose levels, which raises fetal insulin production, resulting in chronic fetal exposure to high levels of insulin.

Because elevated insulin production requires greater oxygen use this may result in depleted oxygen supply for the fetus. Diabetes also may result in fetal iron deficiency. Both conditions can adversely affect fetal brain development, the authors said.

“The sequence of events related to poorly regulated maternal glucose levels is one potential biological mechanism that may play a role in adverse fetal development in the presence of maternal metabolic conditions,” Krakowiak said.

Maternal inflammation, which accompanies metabolic conditions, may also adversely affect fetal development. Certain proteins involved in cell signaling that are produced by cells of the immune system can cross the placenta from the mother to the fetus and disturb brain development.

Other study authors are Irva Hertz-Picciotto, Cheryl Walker, Alice Baker, Sally Ozonoff and Robin Hansen of the UC Davis MIND Institute and Andrew Bremer of UC Davis and Vanderbilt University.

The study was supported by the National Institutes of Health (P01 ES11269 and R01 ES015359), the U.S. Environmental Protection Agency through the Science to Achieve Results (STAR) program (R829388 and R833292), and the UC Davis MIND Institute.

Link Between High Cholesterol and Alzheimer’s Disease Revealed in New Study

Interesting article from Science Daily identifying the link between high cholesterol and a possible link to developing Alzheimer’s Disease: yet another reason to make sure you keep your Leptin levels balanced…

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Rob

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ScienceDaily (Sep. 12, 2011) — People with high cholesterol may have a higher risk of developing Alzheimer’s disease, according to a study published in the September 13, 2011, issue of Neurology®, the medical journal of the American Academy of Neurology.


“We found that high cholesterol levels were significantly related to brain plaques associated with Alzheimer’s disease,” said study author Kensuke Sasaki, MD, PhD, of Kyushu University in Fukuoka, Japan.

For the study, the cholesterol levels were tested for 2,587 people age 40 to 79 who had no signs of Alzheimer’s disease. Then they examined 147 autopsied people who died after a long observation period (10 to 15 years). Of those, 50 people, or 34 percent, had been diagnosed with dementia before death.

The autopsies looked for plaques and tangles in the brain, both known to be trademark signs of Alzheimer’s disease. Plaques are an accumulation of a form of the protein amyloid, which occurs between nerve cells. Tangles are an accumulation of a different protein, called tau, which occurs inside nerve cells.

People with high cholesterol levels, defined by a reading of more than 5.8 mmol/L, had significantly more brain plaques when compared to those with normal or lower cholesterol levels. A total of 86 percent of people with high cholesterol had brain plaques, compared with only 62 percent of people with low cholesterol levels.

The study found no link between high cholesterol and the tangles that develop in the brain with Alzheimer’s disease.

In addition to high cholesterol increasing the risk of Alzheimer’s disease, Sasaki previously found that insulin resistance, a sign of diabetes, may be another risk factor for brain plaques associated with Alzheimer’s disease.

“Our study clearly makes the point that high cholesterol may contribute directly or indirectly to plaques in the brain,” Sasaki said, “but failed treatment trials of cholesterol-lowering drugs in Alzheimer’s disease means there is no simple link between lowering cholesterol and preventing Alzheimer’s.”

This study was supported by the Japan Society for the Promotion of Science and the Japanese Ministry of Health, Labor and Welfare.

Research Offers Insight to How Fructose Causes Obesity and Other Illnesses

Great article from Science Daily on fructose and how it causes obesity and other illnesses….

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Rob

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ScienceDaily (Feb. 27, 2012) — A group of scientists from across the world have come together in a just-published study that provides new insights into how fructose causes obesity and metabolic syndrome, more commonly known as diabetes. In this study which was performed in lab animals, researchers found that fructose can be metabolized by an enzyme that exists in two forms. One form appears to be responsible for causing how fructose causes fatty liver, obesity, and insulin resistance. The other form may actually protect animals from developing these features in response to sugar.


These studies may provide important insights into the cause of the prediabetic condition known as “metabolic syndrome,” which currently affects more than one-quarter of adults in the United States.

The study, “Opposing effects of fructokinase C and A isoforms on fructose-induced metabolic syndrome in mice” was just published in the journal Proceedings of the National Academy of Sciences. Richard Johnson, MD, the senior author of the study and Chief of the Division of Renal Diseases and Hypertension at the University of Colorado School of Medicine said the findings are significant because we now have a better understanding of how fructose causes obesity and other illnesses.

“These studies provide new insights into how fructose may contribute to the development of obesity and diabetes. In particular, the identification of contrasting roles for two enzymes that are involved in fructose metabolism was surprising and could be important in understanding why some individuals may be more sensitive to the metabolic effects of fructose than others.”

Previous research has shown that fructose intake in added sugars such as sucrose and high fructose corn syrup is strongly linked to the epidemic rise in obesity and nonalcoholic fatty liver disease. Fructose intake also causes features of metabolic syndrome in laboratory animals and humans. It is known to cause visceral (organ) fat accumulation and insulin resistance compared to starch based diets even when calories are kept even.

Faculty at the University of Colorado School of Medicine work to advance science and improve care. These faculty members include physicians, educators and scientists at University of Colorado Hospital, Children’s Hospital Colorado, Denver Health, National Jewish Health, and the Denver Veterans Affairs Medical Center. Degrees offered by the CU Denver School of Medicine include doctor of medicine, doctor of physical therapy, and masters of physician assistant studies.

Time Lived With Obesity Linked With Mortality

Good article from Science Daily on the link between mortality and obesity….

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Rob

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ScienceDaily (Mar. 21, 2011) — Monash University researchers have found the number of years individuals live with obesity is directly associated with the risk of mortality.


The research shows that the duration of obesity is a strong predictor of mortality, independent of the actual level of Body Mass Index (BMI). As the onset of obesity occurs earlier and the number of years lived with obesity increases, the risk of mortality associated with adult obesity in contemporary populations is expected to increase compared with previous decades.

Using data from the Framingham Heart Study, 5209 participants were followed up for 48 years from 1948. The current study however only included participants who were free from pre-existing diseases of diabetes, cardiovascular diseases and cancer.

The research showed that for those who had a medium number of years lived with obesity (between five years and 14.9 years), the risk of mortality more than doubled than for those who had never been obese. The risk of mortality almost tripled for those with the longest duration of obesity (more than 15 years).

Furthermore, the research showed for every additional two years lived with obesity, the risk of mortality increased by between six and seven per cent.

“Before now, we did not know whether being obese for longer was any worse for you health than simply being obese. However, this research shows for the first time that being obese for longer increases your risk of mortality, no matter how heavy you actually are,” Monash University researcher, Dr Anna Peeters said.

“This research provides added support for all the current policy trying to prevent obesity in general. It also indicates that we should try extra hard to prevent obesity at younger ages,” said Dr Peeters.

The research was undertaken by Asnawi Abdullah, Rory Wolfe, Johannes Stoelwinder, Christopher Stevenson, Helen Walls and Anna Peeters from Monash University and Maximilian de Courten from the University of Copenhagen.

Insulin Resistance, Type 2 Diabetes Linked to Plaques Associated With Alzheimer’s Disease

As documented in this article from Science Daily, here is another reason to get your Leptin levels and inflammation under control: there is no doubt that inflammation which goes hand in hand with weight gain and insulin resistance contributes to the development of different forms of dementia….

Regards,

Rob

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ScienceDaily (Aug. 25, 2010) — People with insulin resistance and type 2 diabetes appear to be at an increased risk of developing plaques in the brain that are associated with Alzheimer’s disease, according to new research published in the August 25, 2010, issue of Neurology®, the medical journal of the American Academy of Neurology.


Insulin resistance, or the stage before diabetes, happens when insulin, a hormone in the body, becomes less effective in lowering blood sugar.

“Type 2 diabetes and Alzheimer’s disease are two epidemics growing at alarming levels around the world,” said study author Kensuke Sasaki, MD, PhD, with Kyushu University in Fukuoka, Japan. “With the rising obesity rates and the fact that obesity is related to the rise in type 2 diabetes, these results are very concerning.”

The study involved 135 people with an average age of 67 from Hisayama, Japan. The participants had several diabetes glucose tests to measure blood sugar levels. They were also monitored for symptoms of Alzheimer’s disease over the next 10 to 15 years. During that time, about 16 percent developed Alzheimer’s disease.

After the participants died, researchers examined their autopsied brains for the physical signs of Alzheimer’s disease, called plaques and tangles. While 16 percent had symptoms of Alzheimer’s disease while alive, a total of 65 percent had plaques.

The study found that people who had abnormal results on three tests of blood sugar control had an increased risk of developing plaques. Plaques were found in 72 percent of people with insulin resistance and 62 percent of people with no indication of insulin resistance. However, the study did not find a link between diabetes factors and tangles in the brain.

“Further studies are needed to determine if insulin resistance is a cause of the development of these plaques,” said Sasaki. “It’s possible that by controlling or preventing diabetes, we might also be helping to prevent Alzheimer’s disease.”

How Vitamin D Inhibits Inflammation

Inflammation is an important component of leptin resistance and weight gain.

We have all heard about the many benefits of Vitamin D: well here is another one, as documented in this article from Science Daily.  So if you want to lose weight, make sure you address leptin resistance (one of the key targets of our LeptiThin Leptin Resistance / Healthy Weight Management product) – and make sure you are getting enough Vitamin D…

The best way to ensure adequate levels of Vitamin D is through (healthy) sunlight exposure, and if you live in a place like we do here in Vancouver, make sure you take some supplemental Vitamin D in the winter.

Many people can develop absorption problems with Vitamin D as they age, so the only sure way to check on adequate Vitamin D levels is to get your levels tested through a lab analysis…

Regards,

Rob

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ScienceDaily (Feb. 23, 2012) — Researchers at National Jewish Health have discovered specific molecular and signaling events by which vitamin D inhibits inflammation. In their experiments, they showed that low levels of Vitamin D, comparable to levels found in millions of people, failed to inhibit the inflammatory cascade, while levels considered adequate did inhibit inflammatory signaling. They reported their results in the March 1, 2012, issue of The Journal of Immunology.


“This study goes beyond previous associations of vitamin D with various health outcomes. It outlines a clear chain of cellular events, from the binding of DNA, through a specific signaling pathway, to the reduction of proteins known to trigger inflammation,” said lead author Elena Goleva, assistant professor of pediatrics at National Jewish Health. “Patients with chronic inflammatory diseases, such as asthma, arthritis and prostate cancer, who are vitamin D deficient, may benefit from vitamin D supplementation to get their serum vitamin D levels above 30 nanograms/milliliter.”

Current national guidelines suggest that people should maintain a minimum blood serum level of 20 ng/ml, although there is much scientific debate about optimum levels. Vitamin D has long been known to contribute to bone health by promoting the absorption of calcium. In recent years, much attention has been paid to its possible immune and inflammatory benefits. Low vitamin D levels have been associated with several diseases including asthma, cancer, diabetes, and arthritis.

In the current study researchers examined the specific mechanisms by which vitamin D might act on immune and inflammatory pathways. They incubated human white blood cells with varying levels of vitamin D, then exposed them to lipopolysaccharide (LPS), a molecule associated with bacterial cell walls that is known to promote intense inflammatory responses.

Cells incubated with no vitamin D and in solution containing 15 ng/ml of vitamin D produced high levels of cytokines IL-6 and TNF-alpha, major actors in the inflammatory response. Cells incubated in 30 ng/ml vitamin D and above showed significantly reduced response to the LPS. The highest levels of inflammatory inhibition occurred at 50 ng/ml.

Through a complex series of experiments, the researchers identified a new location where the vitamin-D receptor appears to bind directly to DNA and activate a gene known as MKP-1. MKP-1 interferes with the inflammatory cascade triggered by LPS, which includes a molecule known as p38, and results in higher levels of IL-6 and TNF-alpha.

“This newly identified DNA-binding site for the vitamin-D receptor, and the specific pathways inhibited by higher levels of vitamin D provide a plausible mechanism for many of the benefits that have been associated with vitamin D,” said Dr. Goleva. ‘The fact that we showed a dose-dependent and varying response to levels commonly found in humans also adds weight to the argument for vitamin D’s role in immune and inflammatory conditions.”

Is Your Gut Leaky?

Here is a great article from Balanced Bites on the whole concept of Leaky Gut Syndrome…which can cause many diverse – and potentially serious – negative health consequences…

Regards,

Rob

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LeptiThin: Leptin Resistance / Healthy Weight Loss

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If I told you that I ate an omelette for breakfast, a slice of quiche for lunch and then dined out on souffle for dinner, you might ask me, “isn’t that a lot of eggs?” But what if I told you I ate a bowl of cereal for breakfast, a sandwich for lunch and some pizza or pasta for dinner? The question “isn’t that a lot of wheat?” would likely not leave your mouth. We’re so accustomed to grain-based, refined foods appearing at every meal, that we seldom stop to ask if we’re overdoing it.

Sure, I eat eggs almost every day. But do I eat them at every meal? Not even close. And yes, I’d be sad if someone told me I could no longer eat them. And yes, there are many people who are allergic to eggs. But what about the people who are allergic to grains? The thing about most food allergies or intolerances is that they typically result in identifiable types of discomfort to the eater. Those who have suffered with lactose intolerance can tell you how it feels shortly after they eat the offending dairy product. That said, many people also experience similar discomfort after eating grains, particularly gluten-containing grains. And while those feelings may be enough for many people to avoid grains, the larger issue with a gluten or grain intolerance is that many of the symptoms are NOT easily identified by the eater as being related.

Gluten (more specifically the protein in gluten called gliadin) can cause a myriad of health problems, but they aren’t always obviously related to the fact that the you’ve consumed grains. In fact, they don’t always occur immediately after eating them. When digestive issues occur, often it isn’t until you stop eating gluten for at least two weeks, allow your body recover from the attack it’s been under, and then reintroduce the offending foods. Once your body has had a chance to rebalance, the offending foods often result in direct discomfort. You might think you made yourself intolerant by eliminating the gluten, but that’s not how it works.

What if you never stop eating the offending foods? Does that mean the allergy or intolerance isn’t there? If you don’t eliminate then reintroduce the food to FEEL the effect of it, can you simply avoid the negative effects? Unfortunately, it’s not that simple. This is where the chronic, negative effects of a gluten or grain intolerance really wreak havoc. It’s the effects of gluten that you don’t feel immediately that are far worse than the ones that you do feel.

Dangerous Grains: Why Gluten Cereal Grains May Be Hazardous To Your Health
Check this book
out for more info
on gluten!

Sure, digestive discomfort is something most of us would choose to avoid if possible, but what about some of the other gluten associated medical conditions that can arise? According to Dr. James Braly and Ron Hoggan, authors of “Dangerous Grains: Why Gluten Cereal Grains May Be Hazardous to Your Health,” the list of these conditions is seemingly endless. Maybe you can identify with one (or more) of the conditions they cite as showing an association to gluten consumption. While this is an abbreviated list, it’s worthwhile for anyone who feels sub-optimal to consider eliminating post-agricultural revolution calorie-sources (aka: grains, specifically gluten-containing forms) from our diets.

  • chronic joint pain
  • bloating
  • weight gain or unwanted weight loss
  • psychological disorders such as depression and anxiety
  • fatigue
  • Attention Deficit Disorder (ADD)
  • anemia
  • asthma
  • canker sores (mouth ulcers or sores)
  • Type 1 Diabetes: Insulin Dependent Diabetes Mellitus (IDDM)
  • IBS
  • Pre-and Post-Natal difficulties including: difficulty with breast feeding, infertility, miscarriages, and various obstetrical disorders
  • bone diseases, calcium deficiency
  • cancer
  • epilepsy
  • migraines
  • dyslexia
  • edema
  • gallbladder malfunction
  • gastric ulcers
  • amenorrhea
  • alopecia
  • heart disease
  • liver disease
  • lupus
  • pancreatitis
  • rheumatoid arthritis
  • skin diseases like eczema, psoriasis and dermatitis herpetiformis
  • lactose intolerance
  • thyroid disease- hypo and hyperthyroidism
  • ulcerative colitis
  • vitamin or mineral deficiencies
  • vitilago

I didn’t list nearly all that are in the book. If you’re interested, check it out for yourself or do some searching online. Seriously, the list is pretty comprehensive. That’s not to say that gluten alone is responsible for all of those problems, but it certainly can be. I don’t know about you, but if I learned that something I was eating all the time was the cause of major discomfort or disease in my life, I’d give some serious thought to developing a diet for myself that eliminates that food.
I know what you’re thinking…”but how can a FOOD be responsible for these diseases?” Well, the mechanisms by which these diseases are triggered nearly all begin in our gut. Yes, in our digestive system. In fact, according to Elizabeth Lipski, Ph. D, CCN, author of “Digestive Wellness” and “Digestive Wellness for Children,” “In addition to obvious digestive troubles, many other medical problems are caused by faulty digestion.”
Often we are lacking the enzymes needed to break down the specific proteins. This is most easily understood in the case of lactose intolerance and the addition many people make of a lactase enzyme to their diet or to their milk to enable their bodies to handle those foods. When we consume foods that our bodies are not able to properly digest and assimilate, these foods (specifically the proteins in them) are seen as invaders to our immune system. The undigested proteins are larger particles than our gut lining is able to absorb and the microvilli are irritated by these particles. What typically results from this irritation are tiny tears in our gut lining that then allow those undigested food proteins to escape our digestive system and enter our bloodstream.

According to Mark Sisson, author of “The Primal Blueprint,” (a fantastic read, by the way) in his April 28th, 2010 interview on Underground Wellness Radio,

“When larger undigested protein molecules enter the bloodstream, your body goes to work. Your immune says, ‘hey, this isn’t an amino acid, this is actually a full-on protein. It might be a virus. It might be a bacteria. I better set up an immune response to fight it.’ So the immune system starts to set up a response to these large, undigested protein molecules that enter the bloodstream. That would be okay, but for the fact that some of these protein molecules resemble the same protein molecules that reside on the outside of cell membranes in certain parts of the body… In some of your joints, there are cell membranes that have proteins that may resemble some of the proteins that your body just set up an immune response to… your immune system does not know which is the enemy and which is friendly, which is you. So it fights them all. As a result of your having introduced these foreign proteins into the bloodstream that happen to resembles ones that you have that are actually friendly, your immune system starts to attack you. And that may manifest itself with an autoimmune disease… it may be something like rheumitoid arthritis… it may be Type 1 Diabetes at the age of 25 or 30… and there are several other versions of autoimmune diseases that probably, most likely, have a dietary origin.”

Lipski corroborates Sisson’s explanation when she states that:

“When the intestinal lining is damaged even more, substances larger than particle size —  disease-causing bacteria, potentially toxic molecules, and undigested food particles — are allowed to pass directly through the weakened cell membranes. They go directly into the bloodstream, activating antibodies and alarm substances called cytokines. The cytokines alert our lymphocytes (white blood cells) to battle the particles. Oxidants are produced in the battle, causing irritation and inflammation far from the digestive system. That is the basis for a condition called increased intestinal permeability or leaky gut syndrome.”

You can certainly create a test for yourself and eliminate gluten from your diet, or even all grains, for a time period of at least two weeks and see how you feel while not eating them as well as how you feel when you start eating them again. Often people feel like they’re having withdrawal symptoms when they stop, which can be an indication of an intolerance, and then also uncomfortable symptoms when they resume.

Lipski explains this process in more detail in “Digestive Wellness,” and I’d highly recommend picking up a copy of the book if you’re interested in understanding more about the mechanism as well as various approaches to healing the gut.  Of course, if you’d like help in this process, contact me for 1:1 coaching and we can work together. I’ll teach you how to create an elimination diet to find out if you are sensitive to gluten and whether you should be avoiding it. Trust me, there are limitless possibilities and combinations of foods to eat that don’t include gluten that look, smell and taste fantastic. It can seem daunting at first to toss aside many foods you’re used to eating, but with help, it’s all possible.

The Primal Blueprint: Reprogram your genes for effortless weight loss, vibrant health, and boundless energy
A great read
by Mark Sisson
Digestive Wellness: How to Strengthen the Immune System and Prevent Disease Through Healthy Digestion (3rd Edition): Completely Revised and Updated Third Edition
A fantastic resource
by Elizabeth Lipski

Enjoy & be well!
Diane Sanfilippo
BS, Certified Nutrition Educator, C.H.E.K. Holistic Lifestyle Coach
San Francisco Nutritionist serving the Bay Area and beyond via phone & Skype consultations.

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Link Between High Cholesterol and Alzheimer’s Disease Revealed in New Study

Here is a good article from Science Daily on the link between high cholesterol and Alzheimer’s Disease.

This is another reason why keeping leptin levels in balance is important: leptin resistance will cause issues with insulin, cholesterol and many other things…

Regards,

Rob

The TRUTH is Out There

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ScienceDaily (Sep. 12, 2011) — People with high cholesterol may have a higher risk of developing Alzheimer’s disease, according to a study published in the September 13, 2011, issue of Neurology®, the medical journal of the American Academy of Neurology.


“We found that high cholesterol levels were significantly related to brain plaques associated with Alzheimer’s disease,” said study author Kensuke Sasaki, MD, PhD, of Kyushu University in Fukuoka, Japan.

For the study, the cholesterol levels were tested for 2,587 people age 40 to 79 who had no signs of Alzheimer’s disease. Then they examined 147 autopsied people who died after a long observation period (10 to 15 years). Of those, 50 people, or 34 percent, had been diagnosed with dementia before death.

The autopsies looked for plaques and tangles in the brain, both known to be trademark signs of Alzheimer’s disease. Plaques are an accumulation of a form of the protein amyloid, which occurs between nerve cells. Tangles are an accumulation of a different protein, called tau, which occurs inside nerve cells.

People with high cholesterol levels, defined by a reading of more than 5.8 mmol/L, had significantly more brain plaques when compared to those with normal or lower cholesterol levels. A total of 86 percent of people with high cholesterol had brain plaques, compared with only 62 percent of people with low cholesterol levels.

The study found no link between high cholesterol and the tangles that develop in the brain with Alzheimer’s disease.

In addition to high cholesterol increasing the risk of Alzheimer’s disease, Sasaki previously found that insulin resistance, a sign of diabetes, may be another risk factor for brain plaques associated with Alzheimer’s disease.

“Our study clearly makes the point that high cholesterol may contribute directly or indirectly to plaques in the brain,” Sasaki said, “but failed treatment trials of cholesterol-lowering drugs in Alzheimer’s disease means there is no simple link between lowering cholesterol and preventing Alzheimer’s.”

This study was supported by the Japan Society for the Promotion of Science and the Japanese Ministry of Health, Labor and Welfare.

Ovarian Cancer Risk Related to Inherited Inflammation Genes

Great article from Science Daily talking about research indicating that genes involved in inflammation can increase the risk of ovarian cancer.

Increased inflammation has been found to be involved in the development of some cancers (and will probably be found to be a contributing factor to many more cancers as research continues).

This is one of the benefits of our LeptiThin product: virtually everyone who is overweight or obese has increased levels of inflammation, which goes hand in hand with Leptin resistance.  One of the ways in which LeptiThin works is that it decreases inflammation, which can be a factor in many chronic, degenerative diseases…

Regards,

Rob

The TRUTH is Out There…

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Robert Lamberton Consulting 

Cutting Edge Nutraceutical Product Formulation & Market Development

Holistic Health & Lifestyle Education

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My Holistic Health Blog

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LeptiThin: Leptin Resistance / Healthy Weight Loss

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Email: roblconsulting@gmail.com

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ScienceDaily (Feb. 7, 2012) — In a study conducted by researchers at Moffitt Cancer Center and colleagues from 11 other institutions in the Unites States and the United Kingdom, genes that are known to be involved in inflammation were found to be related to risk of ovarian cancer.


Their study appeared in a recent issue of Cancer Research, published by the American Association for Cancer Research.

Chronic inflammation is known to influence risk of several cancers, including ovarian cancer. The researchers identified 27 genes that are involved in inflammation and sought to determine whether inter-individual differences in these genes were related to risk of ovarian cancer. To do that they determined the frequency of 162 single-nucleotide polymorphisms (SNPs, pronounced “snips”) in DNA extracted from a blood sample provided by approximately 900 women with ovarian cancer (cases) and 1000 cancer-free women (controls). Whenever a SNP is observed it means that there are two forms (alleles) of the gene and the least common one is termed the “minor allele.” The frequency of 21 of the 162 SNPs differed between the cases and controls and was subsequently examined in a larger study that included 3,100 cases and 2,100 controls from five independent studies.

“When we examined the relationship between SNPs in inflammation-related genes and the risk of ovarian cancer, we found variants in five of the 27 genes were related to risk. What was interesting to us was that women who carried the minor alleles had lower ovarian cancer risk. Each SNP appeared to lower risk by about 10 percent,” explained study co-author Thomas A. Sellers, Ph.D., M.P.H., Moffitt executive vice president and director of the Moffitt Research Institute.

One of the genes encodes Interleuken 1 alpha (IL1A), a cytokine, or a small signaling protein molecule that is involved in numerous immune and inflammatory responses, said the authors. IL1A has been associated with many inflammatory response conditions and diseases. In this study, the researchers found that IL1A, and another gene, AloX5, “appear to harbor common inherited variants associated with modest differences in the risk of ovarian cancer.”

“The importance of inflammation pathways in the development of many cancers prompted us to examine this association between SNPS in inflammation-related genes and risk for ovarian cancer,” explained Sellers. “If these results can be confirmed, it might provide insights into how risk may be reduced, through strategies to lower chronic inflammation.”

The authors noted that in 2011 there were an estimated 225,500 new cases of ovarian cancer worldwide. Although some women are at greatly elevated risks of ovarian cancer due to inherited mutations in the BRCA1 and BRCA2 genes, these are rare in the population and account for perhaps 10 percent of cases. However, a substantial portion of genetic influence on ovarian cancer risk has been “unexplained” and some of that may be due to common genetic variants. Sellers points out that “the Il1A variant that was most strongly protective is carried by 30 percent of women in the study, so the impact at the population level is not trivial.”

The Follow-Up of Ovarian Cancer Genetic Association and Interaction Studies (FOCI) is funded by the National Cancer Institute and is based at Moffitt. In addition to researchers from Moffitt, researchers from Columbia University, Duke University, the Mayo Clinic College of Medicine, the University of South Florida, Brigham and Women’s Hospital, the University of Cambridge (UK), the University of Southern California and the Institute of Cancer Research (UK) participated in the study.

Journal Reference:

  1. K. L. White, J. M. Schildkraut, R. T. Palmieri, E. S. Iversen, A. Berchuck, R. A. Vierkant, D. N. Rider, B. Charbonneau, M. S. Cicek, R. Sutphen, M. J. Birrer, P. D. P. Pharoah, H. Song, J. Tyrer, S. A. Gayther, S. J. Ramus, N. Wentzensen, H. P. Yang, M. Garcia-Closas, C. M. Phelan, J. M. Cunningham, B. L. Fridley, T. A. Sellers, E. L. Goode. Ovarian Cancer Risk Associated with Inherited Inflammation-Related Variants. Cancer Research, 2012; DOI: 10.1158/0008-5472.CAN-11-3512

Green tea helps maintain functional ability and prevent cognitive decline as we age

tea

One of the ingredients in our LeptiThin product formulation is Green Tea Extract.  The reason it is included is that it helps with weight loss, however green tea (and its specific active ingredient: EGCG – Epigallocatechin gallate) provides numerous other health benefits.

This article from Natural News documents one of these benefits: the prevention of cognitive decline as we age…

Regards,

Rob

The TRUTH is Out There…

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Robert Lamberton Consulting 

Cutting Edge Nutraceutical Product Formulation & Market Development

Holistic Health & Lifestyle Education

My Website: roblamberton.com

My Holistic Health Blog

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LeptiThin: Leptin Resistance / Healthy Weight Loss

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(NaturalNews) Green tea has long been hailed as a cardio-protective beverage due to its ability to lower levels of oxidized LDL cholesterol, an established heart disease risk factor. It has also been shown to promote brain health because the active compound, EGCG (Epigallocatechin gallate) freely crosses the blood-brain barrier to provide antioxidant support and lower damaging levels of brain inflammation. Researchers from Japan reporting in the American Journal of Clinical Nutrition demonstrate that regular green tea consumption lowers the risk of developing functional disabilities that lead to problems with daily chores and activities, such as bathing or dressing. Drinking up to five cups of green tea each day can lower the risk of developing functional disabilities as we age by nearly one half.

Prior studies have determined that consuming green tea lowers the risk of diseases associated with functional disability, such as osteoporosis, cognitive impairment and stroke. To date, no formal studies have been conducted to confirm the impact of green tea consumption on functional ability. Researchers from Tohoku University Graduate School of Medicine in Japan modeled this study to affirm the positive results associated in the past with drinking green tea.

Daily Green Tea Consumption Significantly Lowers Risk of Functional Decline

To design this research work, scientists handed out questionnaires to nearly 14,000 respondents aged 65 or older. The participants answered questions about general diet, green tea consumption and lifestyle. After a period of five years, researchers were able to find a close inverse link between functional disability risk and the consumption of green tea. Higher intake of green tea was associated with a dramatically lower risk of functional disability in the group studied.

The research team concluded that nearly 13% of the participants consuming the lowest amount of green tea (one cup or less each day) developed moderate to severe degrees of functional disability. By contrast, only 7% of those consuming the highest amount of green tea (5 cups or more each day) were classified with any degree of functional decline. The highest level of green tea consumption was shown to cut the risk of functional and cognitive decline by close to one-half.

The researchers noted that those consuming five or more cups of green tea each day also ate more fruit and vegetables, consumed more fish, were less likely to smoke, had fewer strokes or heart attacks, and tended to have a higher level of education. Improved dietary and lifestyle considerations are synergistic factors that compliment green tea consumption and likely contribute to the positive results in this study. Health-minded individuals already follow strict dietary principles to maintain brain health and functional abilities. Drinking 5 or more cups of green tea each day are shown to boost the healthy benefits associated with proper nutrition and lifestyle.

Sources for this article include:
http://www.ajcn.org/content/early/2012/01/24/ajcn.111.023200.full.pdf
http://www.medicalnewstoday.com/articles/241239.php
http://www.cbsnews.com
http://medicalxpress.com

About the author:
John Phillip is a Health Researcher and Author who writes regularly on the cutting edge use of diet, lifestyle modifications and targeted supplementation to enhance and improve the quality and length of life. John is the author of ‘Your Healthy Weight Loss Plan’, a comprehensive EBook explaining how to use Diet, Exercise, Mind and Targeted Supplementation to achieve your weight loss goal. Visit My Optimal Health Resourceto continue reading the latest health news updates, and to download your Free 48 page copy of ‘Your Healthy Weight Loss Plan’.