Obesity is a Form of Cancer

Lol yea didnt think of that one. Adipose tissue for primarily high-energy storage, evolving into a whole endocrine system (or vice versa). Likewise, nerve cells evolving into entire CNS and for some species like us, a brain, hopefully to use. And even highly specialized nerve cells evolving into melanin to protect from cancer-causing solar radiation.

But obesity as a cancer? Imagine the cure... an actual diet & running it off instead of chemo? FDA would ban all natural cures for fat accumulation.

Originally posted by soficrow
reply to post by nomnom

 

Debunked.

Debunked? You spew unsubstantiated bias and obsolete dogma without a shred of evidence or any single reference.

Care to call out anything in particular?

Everything I said was well evidenced in the scientific literature.

reply to post by tropic

Originally posted by tropic
Lol yea didnt think of that one.

Oh yea I did - wrote about elsewhere and here on this thread a few months ago:

posted on 10/6/12 @ 11:08 AM

Only fat cells (adipocytes) are used to store energy, so other cells never are used for fuel - cancerous or not. More to the point, fat (adipocytes and adipose tissue) is an endocrine organ - it produces hormones essential to body functions and also, produces substances essential to immune function.

Adipose tissue has a metabolic function and acts as an endocrine organ—that is, it produces hormones and secretes them into your bloodstream, through which they travel to affect the function of organs all over your body. In fact, fat tissue produces literally dozens of hormones, including leptin, which controls appetite, and adiponectin, which affects insulin sensitivity and blood sugar levels. Because adipose tissue is now known to be so biologically active, researchers think that it could well play an important role in cardiovascular disease, diabetes, cancer, and other diseases.

Fat cells are also important contributors to your immune system and its inflammatory response. Adipose tissue produces many substances, including free fatty acids and cytokines, proteins that affect cell signaling and behavior. Cytokines have an important role in regulating immune system functions. Scientists have identified dozens of different cytokines produced by fat cells, called adipokines. They include interleukins, tumor necrosis factor, and interferons, which trigger inflammation and respond to infections.

But speaking of evolution, you might be interested in checking out all the evidence showing that obesity is inherited epigenetically. For example, a quick overview:

Minireview: Epigenetic Programming of Diabetes and Obesity: Animal Models

A growing body of evidence suggests that the intrauterine (IU) environment has a significant and lasting effect on the long-term health of the growing fetus and the development of metabolic disease in later life as put forth in the fetal origins of disease hypothesis. Metabolic diseases have been associated with alterations in the epigenome that occur without changes in the DNA sequence, such as cytosine methylation of DNA, histone posttranslational modifications, and micro-RNA. Animal models of epigenetic modifications secondary to an altered IU milieu are an invaluable tool to study the mechanisms that determine the development of metabolic diseases, such as diabetes and obesity. …..

Also see: Minireview: Epigenetics of Obesity and Diabetes in Humans

The rapid increase in incidence of obesity over the past two decades cannot be explained solely by genetic and adult lifestyle factors. There is now considerable evidence that the fetal and early postnatal environments also strongly influence the risk of developing obesity in later life. …The mechanism by which the maternal nutritional environment induces such changes is beginning to be understood and involves the altered epigenetic regulation of specific genes. In this review, we discuss the recent evidence that shows that early-life environment can induce altered epigenetic regulation leading to the induction of an altered phenotype. …

Developmental and epigenetic pathways to obesity: an evolutionary-developmental perspective

Also of note:

2006: Cancer is nowadays recognised as a genetic and epigenetic disease.

**
…epigenetic changes, particularly DNA methylation, are susceptible to change and are excellent candidates to explain how certain environmental factors may increase the risk of cancer.

**

Cancer an Epigenetic Disease

Cancers are overwhelmingly caused by environmental factors and hence largely preventable; the focus on therapy based on genetic mutations is misplaced

NOTE: I'm not saying individuals have no power to fight obesity - just that the obstacles are far greater and more complex than are being acknowledged here.

reply to post by nomnom

Everything I said was well evidenced in the scientific literature.

Linkies, dearie? ...and you are aware that most every given scientific dogma and assumption (in biology) has been turned on its butt over the past 10-odd years, right?

Originally posted by soficrow
It was a Eureka moment. The kind where you look at well-known facts in a new light. Facts:

1. Fat cells grow out of control in obesity: a) individual cells grow larger and don't die (hypertrophy); and b) fat cells proliferate (hyperplasia);

Fat cells are NOT growing "out of control" - because every human being CAN control their fat with the right nutrition and exercising.

Saying that it's "out of control" is a big joke..."make believe" for obese people that they are not to blame, even if they are KNOWINGLY eating unhealthy/fatening and spend 80% of their days SITTING on a chair?

Fat cells are not "dying" - you BURN OFF CALORIES/FAT with exercise.

If you supply your body more kcal than you actually burn off - you will get fat. Yes..it IS that simple.

Originally posted by soficrow
reply to post by nomnom

 

Everything I said was well evidenced in the scientific literature.

Linkies, dearie? ...and you are aware that most every given scientific dogma and assumption has been turned on its butt over the past 10-odd years, right?

I think that's a bit of an exaggeration. Some things have been proven false, while others are merely incomplete. Still others are standing as they were.

Give me something specific to link ya. Not sure which part you find to be disputable.

Originally posted by soficrow
It was a Eureka moment. The kind where you look at well-known facts in a new light. Facts:

1. Fat cells grow out of control in obesity: a) individual cells grow larger and don't die (hypertrophy); and b) fat cells proliferate (hyperplasia);

2. Individual fat cells that grow out-of-control-larger develop tiny blood vessels that feed the cell (angiogenesis).

...ALL of these characteristics are standard to cancer. No wonder obesity is "associated with cancer" - it IS a form of cancer. Duh.

Before anyone freaks out - obesity obviously is a very slow form of cancer like most skin cancers - my dad had skin cancer for 50 years, and that's NOT what killed him.

Most important, the right diet can heal cancer - good food is not just "healthy," it's medicine.

But let's call a spade a spade.

Does anyone else see this?


Adaptations to environmental stress: Growth alterations

Angiogenesis

On ATS: Infections cause 1 in 6 cancers worldwide

Fat doesn't grow out of control, because weight gain and weight loss are controllable events. If you eat crap and don't do anything, you'll gain fat. If you eat well, and exercise regularly, you can maintain or lose fat.
Its controllable by a simple equation, unlike cancer where there is no equation to prevent or control cancer.

reply to post by flexy123

Fat cells are NOT growing "out of control"

If you follow the links and read the science, you will learn that yes, in fact, they are.

If you're still ...engaged, then you might want to move forward a step and learn a bit about epigenetics.

reply to post by soficrow


I just skimmed that thread. Not sure how you're linking epigenetics to "uncontrolled cell growth".

Their are environmental circumstances that cause epigenetic changes to the individual, or their offspring.

...and what

that means a child may be predisposed towards a propensity to store more energy in fat cells, and once they reach their limit...grow new ones.... and what? that has nothing to do with "cancer" or "uncontrolled cell growth".

We have too much evidence that, regardless of the circumstances which led to the individual becoming obese, they can control their circumstances with much will power, and either maintain their current weight -- stop new cell growth -- , or change their baseline and weight over time.

reply to post by nomnom

....Not sure how you're linking epigenetics to "uncontrolled cell growth".

The science shows obesity results from epigenetics - both cancer and obesity result from epigenetic processes - both cancer and obesity involve "uncontrolled cell growth" or hyperplasia in the early stages

For example, women with higher subcutaneous fat mass exhibited both adipocyte hypertrophy and hyperplasia, whereas increased omental fat was primarily due to hypertrophy(9). Drolet et al. suggest that subcutaneous deposition of fat occurs early in obesity[/url]...

We have too much evidence that, regardless of the circumstances which led to the individual becoming obese, they can control their circumstances with much will power, and either maintain their current weight -- stop new cell growth -- , or change their baseline and weight over time.

From my OP:

Most important, the right diet can heal cancer - good food is not just "healthy," it's medicine.

But let's call a spade a spade.

Does anyone else see this?

I'm not questioning individuals' power to overcome any kind of adversity - just attempting to vilify the common lack of education regarding just how much adversity must be overcome in this circumstance.


.....I should have titled this thread "Obesity: a Cancer of Adipocytes?" It follows (in my mind) from the following heresy:

Atherosclerosis: a cancer of the blood vessels?

A series of molecular pathways have in common a significant role in the pathogenesis and progression of atherosclerosis and cancer. Shared mechanisms implicated for both diseases include oxidative stress and the cellular damage that results from it, toxic metabolites produced by cigarette smoking, and increased dietary fat intake. Atherosclerosis may begin when an injury or infection mutates or transforms a single arterial smooth muscle cell in the progenitor of a proliferative clone, similar to the most widely held carcinogenesis theory. Cell proliferation regulatory pathways have been associated with plaque progression, stenosis, and restenosis after angioplasty and with cancer progression. Alterations in cell adhesion molecules have been linked to plaque formation and thrombosis and to tumor invasion and metastasis. Altered expression of proteases associated with thrombolysis has been implicated in atherosclerotic plaque expansion and hemorrhage and in the invasion and metastasis of malignant neoplasms. Ligand-growth factor receptor interactions have been associated with early atherosclerotic lesions and with cancer development and spread. Nuclear transcription factors have been associated with progression of both diseases. Angiogenesis modulators have been linked to plaque expansion and restenosis of atherosclerotic lesions and to local and metastatic tumor expansion.
PMID: 11993705