Obesity Pandemic - Infectious, or Personal Responsibility?

reply to post by soficrow


See the above. That's not the case.

You're talking about cholesterol production in BRAIN CELLS in the papers that you linked. Most cholesterol is produced and transported from the liver to the peripheral cells, not the other way around. When cells begin to make MORE cholesterol, they simply down-regulate receptor activity to prevent over saturation.

TWO NEW STUDIES ON ASPARTAME AND DIET DRINKS CONFIRM SOURCE OF OBESITY, CANCER/ MALIGNANT BRAIN TUMOR EPIDEMICS. NEUROSURGEON SAYS BAN TOXIN FROM SCHOOLS!
By Dr. Betty Martini...
...Since aspartame can increase obesity and may even cause the metabolic syndrome that affects 48 million Americans, there is no reason to ever consume this product"

www.wnho.net...

So..."diet" (sic) products make you fat and break down into embalming fluid, and poisonous Isopropyl alcohol, and it looks like the stuff causes tumors too...for sure the stuff cause a craving for carbs

The destruction of the insulin process in the body it is beginning to look like a CRITICAL factor in the rise of obesity

advertising has been shown to cause an aversion to healthy food.

proprietary "NATURAL FLAVOURS" contain addictive exitotoxins

TV and videoe games causes addictive brainwave entrainment, which interferes with a health lifestyle.

The food guides promote UNHEALTHY eating habits


at what point does the avrage person have ANY CHOICE at all?

The relationship between naturally occurring low cholesterol concentrations (

reply to post by DevolutionEvolvd


You seem married to the idea of supporting the corporate strategy to prove "bad diet" is the primary cause of obesity and heart disease, at least - and completely resistant to the notion that other factors -like prions- might be more definitive. …I do not have time to make the "prion case" here and now - and am only willing to throw things out for consideration. Sorry, but I will not allow this "blame the victims" strategy to proceed unchallenged.

Despite other factors that are considered high-risk for cardiovascular disease development, those with increased LDL receptor activity had a "substantial reduction" in coronary events.

…..You were associating hypercholesterolemia with increased cellular biosynthesis of cholesterol in brain cells due to prion presence. The reasoning, then, was that Prion Diseases and misfolded proteins were leading to increased cholesterol and hypercholesterolemia. Well, unfortunately, based on the above, this just isn't the case in most cases of hypercholesterolemia, as it's not a CHOLESTEROL issue...it's a Lipoprotein and LDL receptor issue.

No - I wasn't drawing a direct-cause-and-effect linear relationship. That's what you keep pushing for, while I keep insisting the approach is not applicable. …We're looking at overlapping systems, composed of numerous parts, any and all of which are subject to disruption - any of which could create different 'pathways.' I strongly believe it's a huge mistake to look for a standard linear effect, or expect to find one. Moreover, evidence indicates that the processes occurring in nerve and brain cells likely occur in other cells too, with other misfolded proteins, not just the prion protein.

That said, misfolded and wild-type lipoproteins are strongly implicated in prion pathogenesis too, not just prion-created cholesterol. Check it out.

…..prions from the brains of patients with sporadic Creutzfeldt–Jakob disease (CJD) bind to very low-density (VLDL) and low-density (LDL) lipoproteins but not to high-density lipoproteins (HDL) or other plasma components ……apolipoprotein B (apoB), which is the major protein component of VLDL and LDL, bound PrPSc through a highly cooperative process.

For infectious prion protein (designated PrP(Sc)) to act as a template to convert normal cellular protein (PrP(C)) to its distinctive pathogenic conformation, the two forms of prion protein (PrP) must interact closely. The neuronal receptor that rapidly endocytoses PrP(C) is the low-density lipoprotein receptor-related protein 1 (LRP1). We show here that on sensory neurons LRP1 is also the receptor that binds and rapidly endocytoses smaller oligomeric forms of infectious prion fibrils, and recombinant PrP fibrils.

reply to post by Danbones


Aspartame is just one of the many protein-products brought to you with PROTEIN ENGINEERING. Long story short, it's an infectious misfolded protein (aka prions) - one of the very many that are manufactured and sold to us under one guise or another - and make us sick.

It's been going on a long, long time. Long enough that the slow infections they cause are becoming pandemic.

ABOUT PROTEIN ENGINEERING

1989: Redesigning a sweet protein: increased stability and renaturability

This is not the case with aspartame or with other amino acid sweeteners which, when decomposed, elevate specific amino acid pools and could cause adverse effects.

Also see: peds.oxfordjournals.org...

Understanding and increasing protein stability

This review surveys the processes leading to loss of protein function and the types of molecular interaction that help stabilize proteins. It considers the effects of organic solvents on stability and the special features of thermophilic proteins. The deliberate manipulation of stability by protein engineering is discussed using the enzyme subtilisin as example. Both random and rational mutations of this protein have led to variants with greatly improved tolerances of high temperatures and organic solvents. One can also use chemical modification to modify protein stability and some of the main approaches are reviewed. The chemical and genetic strategies are complementary and have been combined to stabilize cytochrome c by metal-mediated cross-linking following site-specific mutagenesis. The article concludes by summarizing the beneficial effects of certain additives on protein stability.

reply to post by DevolutionEvolvd


I thought we already handled the liver association - the liver is the body's "first responder" - and takes the first -and most major- hit from industrial contaminants and pollution; it also builds proteins, and is the location where many proteins first misfold.

The main functions of the liver is to process nutrients from food, make bile, remove toxins from the body and build proteins.

The liver is a vital organ present in vertebrates and some other animals. It has a wide range of functions, including detoxification, protein synthesis, and production of biochemicals necessary for digestion. ……The liver is thought to be responsible for up to 500 separate functions, usually in combination with other systems and organs.

The following articles deal specifically with PrP prions, but other work I can't get to involves other misfolded proteins - notably anti-trypsin and human growth hormone (HGH) as I recall - both linked to a variety of diseases. Misfolded GH alters protein trafficking. 'Tis a tangled web - what can I say?

[url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1866339/]Expression of Cellular Prion Protein in Activated Hepatic Stellate Cells

PrP expression is closely related to stellate cell activation associated with fibrogenic stimuli.

Clinicopathological characterization of prion: a novel marker of activated human hepatic stellate cells.

reply to post by DevolutionEvolvd

Yipes - just discovered the format mess above - too late to edit. Here it is again.

I thought we already handled the liver thing - the liver is the body's "first responder" - and takes the first -and most major- hit from industrial contaminants and pollution; it also builds proteins, and is the location where many proteins first misfold.

The main functions of the liver is to process nutrients from food, make bile, remove toxins from the body and build proteins.

The liver is a vital organ present in vertebrates and some other animals. It has a wide range of functions, including detoxification, protein synthesis, and production of biochemicals necessary for digestion. ……The liver is thought to be responsible for up to 500 separate functions, usually in combination with other systems and organs.

The following articles deal specifically with PrP prions, but other work I can't get to involves other misfolded proteins - notably anti-trypsin and human growth hormone (HGH) as I recall - both linked variety of diseases. Misfolded GH alters protein trafficking. 'Tis a tangled web - what can I say?

Expression of Cellular Prion Protein in Activated Hepatic Stellate Cells

PrP expression is closely related to stellate cell activation associated with fibrogenic stimuli.

Clinicopathological characterization of prion: a novel marker of activated human hepatic stellate cells.

cmon man

didn't your parents teach you to be fit, active and eat a reasonably healthy diet ?

It's worked for me for 30 years.

If I don't eat well, and don't excercise, I gain weight. Not because of any pandemic - but because I AM LAZY.

I've been at both ends of the weight spectrum, and it was all MY doing.

But your little fantasy of big companies making us fat (not really sure what anyone has to gain from that) had me giggling like a school girl. Thanks.

reply to post by Dachende

cmon man

didn't your parents teach you to be fit, active and eat a reasonably healthy diet ?

You really need to lose your assumptions. They don't look good on you. As I said earlier - Real food has healing power - I'm walking proof of that, and also of the fact that lifestyle choices can mitigate underlying disease (delay progression, etc.). I should be dead - or at the very least, really really sick. I'm not - but I'm not "cured" either.

So no - I do not question the benefits of good food, clean air, uncontaminated water, 'natural' products and stress-free living.

But I am saying we're fighting a losing battle - most evident in the fact that chronic disease is being epigenetically inherited by our children, and most visibly manifested by the childhood obesity pandemics.

.....All the "responsible choices" in the world will not turn back this tide unless and until we clean up our planet.



PS. You're welcome.

OBESOGENS

Obesogens are endocrine disruptors -common environmental contaminants- present in personal care products, ordinary cleaners, food, air, soil and water. They have different effects depending on whether or not the individual is exposed as a fetus, and at what specific times during development. Generally, it doesn't take much exposure or a high dose of exposure; common effects include influencing the "creation of fat cells and permanently affecting the nature of adipose tissue, metabolic processes in the body and weight homeostasis." Obesogens do not change DNA, but epigenetic effects can be inherited.

Males and females are affected differently. loam's old thread deals with endocrine disruptors' effects on men: MEN: You are Being Chemically Castrated.

The EU is pushing for regulation:

Hormone disrupting chemicals targeted to prevent chronic disease in the EU

"Endocrine disrupting chemicals are known to affect the human hormone system, often by mimicking or blocking natural human hormones. An exposure today is not only a health threat for the individuals themselves but also for their future children and possibly their grand-children as well,"

Evidence of the harmful effects of EDCs on health, and especially of pre-natal effects as a result of parental exposure, is growing rapidly. Reducing exposure is increasingly seen as a key tool for preventing cancer and other chronic disease.

The concept of endocrine-disrupting substances as “obesogens,” was first described in 2006. Suspected obesogens are typically ubiquitous environmental chemicals that may act at very low levels of exposure and inappropriately influence the creation of fat cells and permanently affect the nature of adipose tissue, metabolic processes in the body and weight homeostasis. ....

....The list of possible obesogenic chemicals noted in recent reviews includes, DES, BPA, phthalates, organotins, PBDEs, polyfluoroalkyl chemicals, and POPs including OC pesticides and PCBs. Effects may occur by multiple mechanisms and may differ if exposure occurs in utero (during development) or during adulthood. ....

…..In a review of endocrine disrupting chemicals and obesity, a long and growing list of chemicals are noted as possible obesogens including:
• The drug diethylstilbesterol (DES) (Most endocrinologists consider that sufficient causal evidence indicates DES as a known obesogen.)
• BPA (used in polycarbonate plastics and to line most food cans). (BPA exhibits multiple toxicological characteristics that are very similar to DES.)
• Phthalates (in soft vinyl products and many cleaners and personal care products)
• Organotins (used in plastics and as pesticides)
• PBDEs (increasingly restricted and/or banned but used extensively as flame retardants in multiple consumer products and thus commonly found in house dust as well as throughout the food chain).
• Polyfluoroalkyl chemicals (used as stain repellents and in non-stick cooking pans and paper).
• OC pesticides (largely banned but environmentally persistent pesticides).
• PCBs (also banned but environmentally persistent industrial chemicals).

...................continued below...................

………….OBESOGENS continued…………

Another literature review of endocrine disruptors as obesogens describes evidence of multiple obesogenic effects that are suspected from environmental pollutants, several pharmaceuticals, and from food components such as phytoestrogens and the sweetening agent glycyrrhetinic acid. Obesogenic effects are suspected via diverse mechanisms as follows:
• Effects may be mediated by metabolic sensors, such as occur on nuclear or membrane hormone receptors with greater effects from fetal or early life exposures.
• Effects may be mediated by sex steroid dysregulation with multiple animal studies indicating possible effects that also appear to depend on both timing of exposure and gender.
• Effects may result from endocrine disruptors interacting with central neuroendocrine signalling that controls the whole body response to daily nutritional fluctuations, including appetite control. One of several of these effects appears to be on thyroid gland regulation of metabolism, another area where greater vulnerability exists during development given the central role played in fetal development by hormones from the maternal thyroid gland.
• Further neuroendocrine effects are suspected within glucocorticoid hormone signalling. This hormone is present in virtually every cell of all vertebrate animals. It is centrally involved in stress responses, in regulating glucose metabolism, in multiple aspects of fetal development, and if elevated during pregnancy, it can adversely affect fetal development. Disruption of glucocorticoid signalling (from stress and undernutrition, and perhaps also from endocrine disrupting chemicals) can contribute to multiple aspects of the metabolic syndrome.

…..the understanding that epigenetic processes occurring perinatally drive these long term health consequences, suggests that similar epigenetic processes are a plausible mechanism for amplifying several environmentally-induced factors that are giving rise to the suddenness of the current obesity epidemic.

Obesity causes? Over eating and no exercise? Of course that is the only causes right?

Do we just pretend that we do not have many other reasons as to why people become obese?

How about we stop and think about the MANY causes of obesity instead of just ONE cause?

Sleep Debt, we get much less sleep than we need, increasing the possibility that we will become obese. If you get less sleep your body metabolism slows down.

Pollution, it changes our hormones, increasing the possibility that we will become obese.

Ever thought about air conditioning and heating? With people controlling their environment with air conditioning and heating we spend less energy keeping our body temperature controlled, increasing the possibility of becoming obese.

Ohhh how about this one LESS SMOKERS. Smoking reduces a persons body weight, when people stop smoking they are more likely to become obese.

Prescription drugs is one cause of obesity.

GENETICS

Studies are showing that the older a woman is when she has a child the more likely that child will be overweight. Studies are still ongoing so the correlation is not understood yet.

Ancestors' environment. Some influences may go back two generations. Environmental changes that made a grandparent obese may "through a fetally driven positive feedback loop" visit obesity on the grandchildren.

Want to be fertile? Be obese, studies prove that obese people are more fertile than lean people.

Viruses, some viruses are showing to cause obesity.

Hormones used in agriculture, ie: GROWTH HORMONES added to our animals are then consumed by us, who then GROW.

How about gut type? Studies are beginning to show that humans have three "gut types", one which is proving to increase obesity.

The list goes on, but sure, let's continue to accuse people of overeating and not exercising.

Yes, I am positive that some people are obese because of overeating and not exercising, I do not believe that this is the cause of the majority of obese cases and NO we should not take children from loving parents because of weight.

Harm None
Peace

Originally posted by soficrow

No - I wasn't drawing a direct-cause-and-effect linear relationship. That's what you keep pushing for, while I keep insisting the approach is not applicable. …We're looking at overlapping systems, composed of numerous parts, any and all of which are subject to disruption - any of which could create different 'pathways.' I strongly believe it's a huge mistake to look for a standard linear effect, or expect to find one.

How much more ambiguous can you get? Using the above statement, your "theory" could be anything. And any observation could be applied to support it...because...THERE IS NO CLEAR DEFINITION OF THE THEORY AND THE MECHANISMS BY WHICH IT CREATES THE DISEASES DESCRIBED IN THIS THREAD.

Ok. Here's what you said in the OP..

Obesity is linked to high cholesterol, and contrary to popular myth, high cholesterol does NOT result primarily from a bad diet and too much dietary fat. In fact, cholesterol is created in the body by disease-causing prions and other infectious misfolded proteins, which need cholesterol to propagate - infectious misfolded proteins hijack infected cells' metabolic machinery, and force them to create cholesterol and other fats. The connection between high cholesterol and prion disease was established by 1995.

Then you followed with 4 different sources discussing cholesterol and such. You very clearly drew a direct cause and effect relationship from something that had no real relationship. You're making things up as you find extremely loose associations through google searches.

Moreover, evidence indicates that the processes occurring in nerve and brain cells likely occur in other cells too, with other misfolded proteins, not just the prion protein.

Either you're not reading your own sources or you're not clearly understanding them. The three sources you linked in the OP about high cholesterol and prion presence stated this:

"Remarkably, only neuronal cells react in this way -- microglia cells exposed to prions do not increase their cholesterol production,"

The ACTUAL evidence suggests that only specific cells, even in the brain, increase cholesterol production as a result of prion presence.

reply to post by soficrow


I love crows by the way, they are some of the smartest people on the planet. This is blaming the victim or rather the slave of serf. Prions come about in cattle after cattle are given a diet containing meat/meat byproducts. IMHO these and other maladies that are emerging as a pandemic are food/ environmentally created. Created by huge psychopathic corporations who's sole justification for existence is to make huge profits. They have no morality. They care not for human life or life of any kind. They will kill us all and destroy the planet. They will be stopped. They must be stopped.

reply to post by soficrow


This doesn't even address the point I'm making. What are you even arguing here? I'll clear it up for ya!

Most cholesterol produced in peripheral cells, as opposed to hepatic cells, is used for intracellular purposes and not transported elsewhere. The liver, however, IS producing cholesterol and transporting it. My point, once again, is that prion-infected neuronal cells are NOT leading to hypercholesterolemia and your trying to find support for your argument, in places where it doesn't exist, by linking processes and conditions that AREN'T ASSOCIATED.

reply to post by DevolutionEvolvd


You keep asking me for a fully developed thesis - I keep saying I won't gonna give it to you. Doesn't mean I don't have one, or that the points I make -or the directions I point to- aren't valid.

I stand by my main point: numerous factors contribute to and/or create obesity, and when you track the molecular impact of each those factors individually, you will find a common mechanism - misfolded or mutant proteins that create disease through gain or loss of function or toxicity.

As reply to amazed
points out, there is a huge variety of causes for obesity - not just one.

My post above focuses on endocrine disruptors, for example - all the chemicals I've checked so far act on proteins. ...Which is one reason why the Developmental Origins of Health and Disease report concludes in part:

…..the understanding that epigenetic processes occurring perinatally drive these long term health consequences, suggests that similar epigenetic processes are a plausible mechanism for amplifying several environmentally-induced factors that are giving rise to the suddenness of the current obesity epidemic.

A little wrench to throw in here.

I have had outrageously high cholesterol since I was in my 20's and Im 5'4" and 120 lbs. High cholesterol and obesity dont necessarily go together, but they sure want you to believe it does so you can take all of these nifty high priced drugs.
Come to find out high cholesterol being the NORM is common in my dads side of the family and none of them are obese except the ones still on the rez eating garbage that the govt tells them is healthy, filling them full of Lipitor, and making everyone follow this idiotic food pyramid that DOES NOT apply to all peoples!

FOr some here.. look a little deeper and speak with those who arent in your specific "race" group. See what this nonsense is causing in minority populations. I call it soft genocide and minority population control

reply to post by Advantage


It's well-known that high cholesterol doesn't always result in/accompany obesity. But it's still bad. Really bad, actually. Linked to inflammation, heart disease and early death. Not to mention associated with diabetes. Best to get it under control.

NO WAY do I recommend statins - Lipitor almost destroyed me. But if you can develop a taste for curries (for the turmeric), or make turmeric tea - suck back lots of cinnamon, about 2-3 tablespoons per day - use lots of sage, cumin, drink green tea or even black tea - all these things work by inhibiting prion propagation and reducing inflammation. And they DO work.


PS. Re: it's the norm on your Dad's side. Scan the posts above for "epigenetics" - it helps explain why, and does not make it okay.

(I just deleted a whole post accidentally; here's what I saved.)


I still don't think you have ANY idea how that even happens. And I'm quite certain you have NO IDEA how fat-deposition, fat-oxidation and fuel allocation happen, what drives them and what drives obesity (which are all part of the processes involved in obesity, regardless of prion involvement).

Why should I believe you have any idea when the OP has you trying to link loose associations and completely butchering physiology. You saw the term "high cholesterol" in your google search accompanied with "prion" and it you saw how prions are increasing intracellular cholesterol production in the brain and somehow turned that into prions cause hypercholesterolemia!!!!! That DOESN'T MAKE SENSE.

Originally posted by soficrow


So no - I do not question the benefits of good food, clean air, uncontaminated water, 'natural' products and stress-free living.

And what, exactly, is good food?