Sugar is sucrose. Sucrose is glucose and fructose combined and it is immediately separated in the body by the saliva in your mouth. Glucose is fine for your body, it is the energy storage system that metabolizes into glycogen in the liver. Fructose, on the other hand, is a toxin that is metabolized in the body similarly to alcohol, as ChaosEngine said. Essentially it is treated as a toxin and turned into numerous by-products which do things like: delay your leptin response (you feel full later, thus making you eat more), increase your high-density lipo-protein (increasing your cholesterol and storing fat in your liver), and decreasing your sensitivity to insulin (leading to type-2 diabetes).

As to what artician said, high-fructose corn syrup and sugar are treated exactly the same in the human body. In fact, here is a list of all of the things that companies call sugar to hide it when it is the exact same thing: brown sugar, caster sugar, fruit sugar, organic sugar (in fact sometimes they just put organic in front of any of these things to make it seem better for you but trust me, it isn't), evaporated cane juice, evaporated cane syrup, high fructose corn syrup, sucrose, glucose-fructose, brown sugar, honey, molasses, golden syrup, high glucose corn syrup, agave/agave nectar, corn sweetener, fruit juice solids, cane syrup solids, fruit juice concentrate, invert sugar, maltodextrin and even fruit juice.

All of the studies done in the last 15 years have shown that sugar is sugar and calories are not calories. All of the kinds of sugar that have quantities of fructose are bad for you, except when they have fiber. This is why fruit is still good for you while fruit juice is the same thing as soda.

The only things that you do not have to avoid as a sugar are these: brown rice syrup, dextrose and glucose. All of these things are completely glucose, no fructose whatsoever. Therefore, they are largely safe. However, large quantities of glucose can give you a large liver because of the stored glycogen.

Some links if you don't believe me:

Comparison: http://www.foods4betterhealth.com/what-evaporated-cane-juice-sugar-vs-evaporated-cane-juice-8645

Aspartame: http://skeptoid.com/episodes/4127 ; http://www.sciencebasedmedicine.org/are-artificial-sweeteners-safe/

HFCS vs Sugar: http://skeptoid.com/episodes/4157

Dangers of Fructose: http://www.sciencebasedmedicine.org/high-fructose-corn-syrup/

High fructose corn sugar is about 55% fructose and 45% glucose.
"Table sugar" ie sucrose is about 50% fructose and 50% glucose.

Glucose is not fine. You gain the same amount of weight regardless of the type of sugar. Glucose can still kill you, but fructose is worse. It has shown some insulin resistance and also increased cholesterol levels.
http://www.webmd.com/heart/metabolic-syndrome/news/20090421/fresh-take-on-fructose-vs-glucose?page=2

HFCS is not much worse for you than table sugar, but it is worse than dextrose(ie d-glucose). Why don't more people use dextrose? It requires 3 times as much dextrose to achieve the same taste as HFCS. I'm still not sure which is worse.

PS: Both HFCS and dextrose are made from corn.

TONS of things cure cancer. All day, every day. Doctors have no clue what cancer is. All they can do is cut, burn, or poison and cross their fingers.

I didn't say Cannabis was THE cure. It is A cure used by thousands with amazing efficacy. Everyone is different.

Here's 60+ studies for your perusal if you insist on the superiority of western scientific research:

"Cannabis, and the cannabinoid compounds found within it, has been shown through a large cannabisplantamount of scientific, peer-reviewed research to be effective at treating a wide variety of cancers, ranging from brain cancer to colon cancer. Below is a list of over 60 studies that demonstrate the vast anti-cancer properties of cannabis.
Studies showing cannabis may combat brain cancer:
Cannabidiol (CBD) inhibits the proliferation and invasion in U87-MG and T98G glioma cells. Study published in the Public Library of Science journal in October 2013.
Tetrahydrocannabinol (THC) can kill cancer cells by causing them to self-digest. Study published in the Journal of Clinical Investigation in September 2013.
CBD is a novel therapeutic target against glioblastoma. Study published in Cancer Research in March 2013.
Local delivery of cannabinoid-filled microparticles inhibits tumor growth in a model of glioblastoma multiforme. Study published in Public Library of Science in January 2013.
Cannabinoid action inhibits the growth of malignant human glioma U87MG cells. Study published in Oncology Reports in July 2012.
Cannabidiol enhances the inhibitory effects of THC on human glioblastoma cell proliferation and survival. Study published in the Molecular Cancer Therapeutics journal in January 2010.
Cannabinoid action induces autophagy-mediated cell death in human glioma cells. Study published in The Journal of Clinical Investigation in May 2009.
Cannabinoids inhibit glioma cell invasion by down-regulating matrix metalloproteinase-2 expression. Study published in Cancer Research in March 2008.
Cannabinoids and gliomas. Study published in Molecular Neurobiology in June 2007.
Cannabinoids inhibit gliomagenesis. Study published in the Journal of Biological Chemistry in March 2007.
A pilot clinical study of THC in patients with recurrent glioblastoma multiforme. The results were published in the British Journal of Cancer in June 2006.
Cannabidiol inhibits human glioma cell migration through an independent cannabinoid receptor mechanism. Study published in the British Journal of Pharmacology in April 2005.
Cannabinoids inhibit the vascular endothelial growth factor pathway (VEGF) in gliomas. Study published in the Journal of Cancer Research in August 2004.
Antitumor effects of cannabidiol, a nonpsychoactive cannabinoid, on human glioma cell lines. Study published in the Journal of Pharmacology in November 2003.
Inhibition of glioma growth in vivo by selective activation of the CB2 cannabinoid receptor. Study published in the Journal of Cancer Research in August 2001.
Studies showing cannabis may combat colorectal cancer:
Cannabigerol (CBG) can inhibit colon cancer cells. Study published in the Oxford journal Carcinogenesis in October 2014.
Inhibition of colon carcinogenesis by a standardised Cannabis Sativa extract with high content of CBD. Study published in Phytomedecine in December 2013.
Chemopreventive effect of the non-psychotropic phytocannabinoid CBD on colon cancer. Study published in the Journal of Molecular Medecine in August 2012.
Cannabinoids against intestinal inflammation and cancer. Study published in Pharmacology Research in August 2009.
Action of cannabinoid receptors on colorectal tumor growth. Study published by the Cancer Center of the University of Texas in July 2008.
Studies showing cannabis may combat blood cancer:
The effects of cannabidiol and its synergism with bortezomib in multiple myeloma cell lines. Study published in the International Journal of Cancer in December 2013.
Enhancing the activity of CBD and other cannabinoids against leukaemia. Study published in Anticancer Research in October 2013.
Cannabis extract treatment for terminal acute lymphoblastic leukemia of Philadelphia chromosome (Ph1). Study published in Case Reports in Oncology in September 2013.
Expression of type 1 and type 2 cannabinoid receptors in lymphoma. Study published in the International Journal of Cancer in June 2008.
Cannabinoid action in mantle cell lymphoma. Study published in Molecular Pharmacology in November 2006.
THC-induced apoptosis in Jurkat leukemia. Study published in Molecular Cancer Research in August 2006.
Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease. Study published in Blood American Society of Hemmatology in July 2002.
Studies showing cannabis can combat lung cancer:
Cannabinoids increase lung cancer cell lysis by lymphokine-activated killer cells via upregulation of Icam-1. Study published in Biochemical Pharmacology in July 2014.
Cannabinoids inhibit angiogenic capacities of endothelial cells via release of tissue inhibitor of matrix metalloproteinases-1 from lung cancer cells. Study published in Biochemical Pharmacology in June 2014.
COX-2 and PPAR-γ confer CBD-induced apoptosis of human lung cancer cells. Study published in Molecular Cancer Therapeutics in January 2013.
CBD inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1. Study published in the Journal of the Federation of American Societies for Experimental Biology in April 2012.
Cannabinoid receptors, CB1 and CB2, as novel targets for inhibition of non–small cell lung cancer growth and metastasis. Study published in Cancer Prevention Research in January 2011.
THC inhibits epithelial growth factor-induced (EGF) lung cancer cell migration in vitro as well as its growth and metastasis in vivo. Study published in the journal Oncogene in July 2007.
Studies showing cannabis may combat stomach cancer:
Cannabinoid receptor agonist as an alternative drug in 5-Fluorouracil-resistant gastric cancer cells. Study published in Anticancer Research in June 2013.
Antiproliferative mechanism of a cannabinoid agonist by cell cycle arrest in human gastric cancer cells. Study published in the Journal of Cellular Biochemistry in March 2011.
Studies showing cannabis may combat prostrate cancer:
Cannabinoids can treat prostate cancer. Study published by the National Institute of Health in October 2013.
Non-THC cannabinoids inhibit prostate carcinoma growth in vitro and in vivo: pro-apoptotic effects and underlying mechanisms. Study published in the British Journal of Pharmacology in December 2012.
The role of cannabinoids in prostate cancer: Basic science perspective and potential clinical applications. Study published in the Indian Journal of Urology in January 2012.
Induction of apoptosis by cannabinoids in prostate and colon cancer cells is phosphatase dependent. Study published in Anticancer Research in November 2011.
Studies showing cannabis may combat liver cancer:
Involvement of PPARγ in the antitumoral action of cannabinoids on hepatocellular carcinoma (CHC). Study published in Cell Death and Disease in May 2013.
Evaluation of anti-invasion effect of cannabinoids on human hepatocarcinoma cells. Study published on the site Informa Healthcare in February 2013.
Antitumoral action of cannabinoids on hepatocellular carcinoma. Study published in Cell Death and Differentiation in April 2011.
Studies showing cannabis may combat pancreatic cancer:
Cannabinoids inhibit energetic metabolism and induce autophagy in pancreatic cancer cells. Study published in Cell Death and Disease in June 2013.
Cannabinoids Induce apoptosis of pancreatic tumor cells. Study published in Cancer Research in July 2006.
Studies showing cannabis may combat skin cancer:
Cannabinoid receptor activiation can combat skin cancer. Study published by the National Institute of Health in October 2013.
Cannabinoids were found to reduce skin cancer by 90% in just 2 weeks. Study published in the Journal of Pharmacy and Pharmacology in July 2013.
Cannabinoid receptors as novel targets for the treatment of melanoma. Study published in the Journal of the Federation of American Societies for Experimental Biology in December 2006.
Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. Study published in the Journal of Clinical Investigation, in January 2003.
Studies showing cannabis may combat other types of cancer:
Bladder: Marijuana reduces the risk of bladder cancer. Study published in the Medscape site in May 2013.
Kaposi sarcoma: Cannabidiol inhibits growth and induces programmed cell death in Kaposi sarcoma–associated herpesvirus-infected endothelium. Study published in the journal Genes & Cancer in July 2012.
Nose, mouth, throat, ear: Cannabinoids like THC inhibit cellular respiration of human oral cancer cells. Study by the Department of Pediatrics at the State University of New York, published in June 2010.
Bile duct: The dual effects of THC on cholangiocarcinoma cells: anti-invasion activity at low concentration and apoptosis induction at high concentration. Study published in Cancer Investigation in May 2010.
Ovaries: Cannabinoid receptors as a target for therapy of ovarian cancer. Study published on the American Association for Cancer Research website in 2006.
Preparation and characterisation of biodegradable microparticles filled with THC and their antitumor efficacy on cancer cell lines. Study published in the Journal of Drug Targeting in September 2013.
CBD Cannabidiol as a potential anticancer drug. Study published in the British Journal of Pharmacology in February 2013.
Cannabinoids as anticancer modulators. Study published in the Progress in Lipid Research journal in January 2013.
CBD inhibits angiogenesis by multiple mechanisms. Study published in the British Journal of Pharmacology in November 2012.
Towards the use of cannabinoids as antitumour agents. Study published in Nature in June 2012.
Cannabinoid-associated cell death mechanisms in tumor models. Study published in the International Journal of Oncology in May 2012.
Cannabinoids, endocannabinoids and cancer. Study published in Cancer Metastasis Reviews in December 2011.
The endocannabinoid system and cancer: therapeutic implication. Study published in the British Journal of Pharmacology in July 2011.
This list was compiled in part by Alchimiaweb.com.
– TheJointBlog"

If it were done as a single nerve in a direct route, it would be subject to damage from a jerking head motion. This way, the slack (and bundling) adds protection to individual nerves. And again, it works just fine, in ALL mammals.

Let's coin a new term. How about 'stress relief'?

Another point. The heart is functional before it descends into an expanding chest cavity, taking ancillary nerves along for the ride.

And lastly, the evidence points to incremental phenotypic alterations along with some jumps here and there. The first is indicative of environmental adaptations, with possible genetic manipulations [ID] on occasion.

In fact, we ourselves are on the cusp of being able to alter phenotypic outcomes, by PCR, electrophoresis, and subsequent spicing to alter structures and codes. For our progress at this point, search 'genetic engineering'.

While not proof of prior gene altering to alter phenotypes, it is at least evidence that it can be done, while at this juncture, no substantiating evidence exists for random mutations, HGT, and genetic drift to radically alter body plans. Just for minor quantitative adaptive alterations [pigmentation, bone density, fur and hair content, metabolism rates, and yes, cephalic index, essentially brain size increases].

IOW, the evidence clearly points to both microevolution, a likely 'designed-in' function to aid in survival, as well as ID for radical re-designs, possibly by multiple intelligentsia over vast time. Google MDT for more on that possibility.

@JiggaJonson

You may not have said that people lack self-control, but the article you posted indicated as much; that when it comes to food portions, people have difficulty curbing their appetites, and it's simply not true -- and it's seems like a facile excuse for not taking responsibility for oneself.

No one I know who actually wants to lose weight "eats less and exercises" (and I would add "eat healthfully" to that, as well). In fact, I don't know anyone who eats healthfully and exercises regularly and appropriately who is "overweight." (If you know anyone, feel free to put them in touch with me.)

I don't want to get all technical here, but obviously someone who has moldy intestines, "leaky gut," fatty liver, and the resulting blood sugar imbalances may have a difficult time losing weight. And, by no means do I think eating McDonald's is a good idea for any health-conscious person, but individuals need to take some responsibility for educating themselves about their own health. This isn't McDonalds' responsibility.

And yeah, the low fat craze was a bad idea (as I frequently pointed out to many in the 90's), but that's what you get when you trust certain "authorities" to tell you what to do and how to live (especially when it comes from the government and its cronies at the AMA).

If you eat healthfully, your body will tell you when to eat and when to stop. Only a messed up metabolism encourages overeating. For example, the insulin-adrenailne roller-coaster will, of course, have an effect on a person's capacities for immediate self-control. This is why people who binge tend to do so on sweets, wheat, and other no-so-great "foods." Do you know anyone who binges on broccoli? I do not.

So I agree that you need knowledge of what to eat, and this is something that often varies from person to person as we all have different biochemistries, but there are common elements to what more likely agrees with most everyone's health.

(Disclaimer: I am not giving medical advice here, as I have not been licensed by the medical "authorities" to misinform you, but in case you want to know more about the reasons for obesity, I encourage you to check this out for more information: http://www.majidali.com/the1.htm)

Problem is this...

Every drug, used IN MODERATION so as to not be harmful, is [by definition] harmless.

You can't answer a "more/less harmful" question in absolute terms, because individual usage patterns will determine the specific 'harm/danger' posed by each substance.

There is no "standard dosage and regiment + standard metabolism + standard body weight" that you can use to compare substances.
You can pick such numbers, but you'd be pulling them out of your butt.

It's obvious she's giving the stock answer that aligns with her agency's official stance. But even if she were to give a "scientific" response, it would not be black and white.

The answer would be "it depends".
"How much Heroine? How much Coke? How regularly used? etc".

This isn't TV. Just like IRL car crashes rarely result in explosions, IRL drug use rarely results in tragedy.

The simplest example is prescription pain killers. Literally variations on heroine. People are given them for broken ribs, etc. They take them for a while, and then they're done. No harm done.
They could have taken heroine in stead, in the same effective dosage and frequency, and had literally the same experience.

-scheherazade

Adult onset type 2 can be adjusted and your metabolic process stabilized through diet. Once you get your body to the point of insulin-resistance problems (unlike type 1 which is an insulin deficiency without the body's resistance), it's a, "keeping-yourself-in-check" lifestyle for you until you ditch this body and move on to the next....

Type 1?-You may place blame upon your genetic predisposition or injury through drugs or "other", to your pancreatic system.

CBD possesses sedative properties (Carlini and Cunha, 1981), and a clinical
trial showed that it reduces the anxiety and other unpleasant psychological
side effects provoked by pure THC (Zuardi et al. 1982). CBD modulates the
pharmacokinetics of THC by three mechanisms: (1) it has a slight affinity for
cannabinoid receptors (Ki at CB1 = 4350 nM, compared to THC = 41 nM,
Showalter et al. 1996), and it signals receptors as an antagonist or reverse agonist
(Petitet et al. 1998), (2) CBD may modulate signal transduction by perturbing
the fluidity of neuronal membranes, or by remodeling G-proteins that
carry intracellular signals downstream from cannabinoid receptors, and (3)CBD
is a potent inhibitor of cytochrome P450 3A11 metabolism, thus it blocks the
hydroxylation of THC to its 11-hydroxy metabolite (Bornheim et al. 1995).
The 11-hydroxy metabolite is four times more psychoactive than unmetabolized
THC (Browne and Weissman 1981), and four times more immunosuppressive
(Klein et al. 1987).
CBD provides antipsychotic benefits (Zuardi et al. 1995). It increases dopamine
activity, serves as a serotonin uptake inhibitor, and enhances norepinephrine
activity (Banerjee et al. 1975; Poddar and Dewey 1980). CBD protects
neurons from glutamate toxicity and serves as an antioxidant, more potently
than ascorbate and α-tocopherol (Hampson et al. 1998). Auspiciously, CBD
does not decrease acetylcholine (ACh) activity in the brain (Domino 1976;
Cheney et al. 1981). THC, in contrast, reduces hippocampal ACh release in
rats (Carta et al. 1998), and this correlates with loss of short-term memory consolidation.
In the hippocampus THC also inhibits N-methyl-D-aspartate (NMDA)
receptor activity (Misner and Sullivan 1999; Shen and Thayer 1999), and
NMDA synaptic transmission is crucial for memory consolidation (Shimizu et
al. 2000). CBD, unlike THC, does not dampen the firing of hippocampal cells
(Heyser et al. 1993) and does not disrupt learning (Brodkin and Moerschbaecher
1997).
Consroe (1998) presented an excellent review of CBD in neurological disorders.
In some studies, it ameliorates symptoms of Huntington’s disease, such
as dystonia and dyskinesia. CBD mitigates other dystonic conditions, such as
torticollis, in rat studies and uncontrolled human studies. CBD functions as an
anticonvulsant in rats, on a par with phenytoin (Dilantin, a standard antiepileptic
drug).
CBD demonstrated a synergistic benefit in the reduction of intestinal motility
in mice produced by THC (Anderson, Jackson, and Chesher 1974). This
may be an important component of observed benefits of cannabis in inflammatory
bowel diseases.

--"Cannabis and Cannabis Extracts:
Greater Than the Sum of Their Parts?
John M. McPartland
Ethan B. Russo"

tell them that you wont get fat from munchies... apparently, the metabolic changes in a pot users body keeps then skinny ... but, ya know, obesity isnt really a problem in our society.

at all.

Not that this will prove anything for years to come, like I said Science and the medical industry moves SLOOOOOOOWWWWWWWWWWWWWW. When everyone could just be partaking in the most extraordinary human experience that a human can possibly have.

Wiley Online Library has a medical document titled: A critical review of reports of endogenous psychedelic N, N-dimethyltryptamines in humans: 1955–2010

Conclusion: "The answer to the question, ‘Are the tryptamine psychedelic
substances DMT, HDMT and MDMT present in the human body?’
is most likely yes. We believe that the preponderance of the mass
spectral evidence proves, to a scientific certainty, that DMT and
HDMT are indeed endogenous and can be measured in human
body fluids."

Even I was apprehensive as to whether it actually is endogenous. Now I just ask, Why, why, why? Science, baby.

At least there are some in the industry that believe it ought to be known. And for anyone that has ever ingested the grand daddy of psychedelics, of neuromodulation I am sure they were bought and sold on the idea that DMT is a huge discovery:

"Data regarding their peripheral dynamics – concentrations, circadian
variation, and metabolism – as assessed by rigorous
analytic methods applied to biological samples represent the
most accessible approach to beginning to determine their
possible role in human psychophysiology and should be
pursued."

"finally provide us an answer to the question: ‘Why do humans
produce endogenous psychedelics?’ The research thus far is
limited but there are many possibilities awaiting further
inquiry."

Obviously, there simply just is not enough data to suggest how consciousness is affected by these chemicals. Not enough funding, fear of funding, not enough profits to be made. When actually, if they figure out what this stuff is and does it would probably blast open vault door and reveal the secrets of the brain.Or we can just have the status quo and look forward to the next Iphone to cram our heads full of consumer bullshit.

Well said. You couldn't possibly be the bmacs I'm playing words with friends with right now, could you? >> ^bmacs27:

The ultimate issue is "is it a choice?" Homosexuality is not considered a "choice" and thus is not considered "fair game" for criticism. Similarly a lot of data is showing that metabolic set points are not a "choice" or at least they're determined at a young age. Granted, you could starve yourself and exercise into losing weight, but the success rates long term are very low. People who try generally get depressed because they are forcing their body to operate in a way it doesn't want to simply to conform to social norms. The parallels with homosexuality continue. I mean, gay people could act straight. They just don't want to. Further, there is little data to suggest health issues associated with weight once you control for other lifestyle choices (exercise, diet, smoking, etc). Many people exercise everyday, eat a healthy diet, lead healthy lives, and are just fat. Honestly, it's the last bastion of socially accepted prejudice.

Oh, dang. It looks like I missed a great opportunity to dialogue with hpqp about choices and personal responsibility again!

Anyway: Obesity is a disease. It is not "normal". It's a dangerous condition with proven health risks to the individual and demonstrable costs to society.
Obesity is multifactorial. Behavior, metabolic or genetic disorders, societal pressures, and the list goes on...
Regardless of the totality of the condition, behavioral factors are almost always involved, and by their nature are always controllable given adequate motivation. (They're behaviors, after all.) This doesn't mean they're enough by themselves in all cases, but they're a necessary component.
Non-behavioral factors are often controllable with medical intervention. The decision to seek medical intervention is often a controllable behavior. ("Barriers to access" acknowledged.)

I'm typically not one for anecdotal evidence myself, but I don't need to rely on it. There is very little data on successful techniques for long term weight loss. Here's an example. Now, not everyone will interpret these results in the same way that I do. On my reading, people that maintained weight loss needed to check their weight, reduce their fat intake, and expend more energy than people that are naturally weight stable at that weight. In fact, people that lost weight, and regained it had effectively the same habits as people that are weight stable at the lower weight. In other words, weight stable fat people and weight stable thin people exercise and eat the same amounts. Granted, there were some that were able to maintain this increased activity level and highly restrictive diet, however I would suspect if you were to investigate that group you would likely find a higher incidence of psychological issues surrounding body-image, and likely an increased incidence of OCD. Now if your claim is true, the people that lost weight down to an average of 167 pounds or so (the average weight of the weight stable controls), should have been able to have equivalent habits to those controls and maintain that weight as their BMR should be equivalent. Clearly the data shows your claim to be false. They need to maintain an increased activity level and lower fat intake in order to maintain the same weight.

>> ^Duncan:

@bmacs27 You're using every cliche in the book. Basal Metabolic Rates vary in negligible amounts between people of the same gender, age, height, and weight. If your body doesn't get the energy it needs from an outside source, it will break down itself for fuel. And your anecdotal evidence means very little. Argue all you want about how body fat has little to do with health, but don't go saying some people can't lose it (genetic conditions notwithstanding).

@bmacs27 You're using every cliche in the book. Basal Metabolic Rates vary in negligible amounts between people of the same gender, age, height, and weight. If your body doesn't get the energy it needs from an outside source, it will break down itself for fuel. And your anecdotal evidence means very little. Argue all you want about how body fat has little to do with health, but don't go saying some people can't lose it (genetic conditions notwithstanding).

@Duncan And yet this is the commonly suggested course of action for those overweight. Eat 1000-1200 calories a day, and exercise. That's a recipe for disaster. Further, your claim that if you intake fewer calories than you expend you will lose weight. This is not necessarily true. Your body is not a bunsen burner. That's why we have terms like "metabolism" as in so and so has a high metabolism or a low metabolism. In other words, some people can eat and eat and eat, and their body will simply convert the excess energy into heat. For others, that energy is stored as fat. My claim is that there are people for whom prolonged caloric restriction will not result in continued weight loss. Instead the body will continue to store the energy it receives as fat and your brain will be deprived of the energy it needs to allow activity levels necessary to burn anything off. Even with continued restriction. There are cases (e.g. with OCD patients) that prolonged weight loss can be achieved, but often it's simply impossible.

With regards to "life-style change," I agree. It's necessary. However, losing weight isn't. Much more success has been reported encouraging an active lifestyle. Eat until you are sated. That's okay (assuming you don't have a broken sensory system in that regard). People that pursue this approach will usually not lose weight, but they will become healthy. All of their bio-markers (e.g. cholesterol) often come into check. They are active, happy, and healthy. Yet still, people would somehow feel justified sending them a letter telling fatty to get off their ass.

I'll give an example. I watched my girl eat 1200 calories a day for six months. She's 5'2" at 180. The first month of this brought her down to 165/170, but the following five brought her no further. I watched her. She measured every meal with a measuring cup. She's also a geneticist, so she knows a thing or two about the relevant biochem. She was depressed as hell, and her activity level dropped. She was miserable and didn't even really lose substantial weight.

Now, she bikes at least 10-12 hilly miles a day, swims a couple miles three times a week, and does yoga. She eats when she's hungry and stops when she's full. She eats healthily for the most part, but rewards herself with a sweet now and again. Every measure known to correlate with health shows that she is healthy despite her weight. People call her fat all the time. There's just no need. Her doctor doesn't, because many doctors these days know BMI is a bullshit measure. She's not a weird case. I mentioned by buddy the pullup champ in a previous post. The dude was vegetarian in boot camp. He doesn't have an ounce of fat on him, and can do effectively perpetual pushups. He's technically "obese." For a medical term, it's about as useful as "idiot."

The fact is evidence is mounting that your disposition towards retaining fat probably has more to do with what was eaten by your mother during pregnancy than anything you do in your lifetime (other than maybe early childhood). Your body has a weight it would like to keep, and it will succeed in keeping it. If people would just change the societal pressure towards becoming healthy rather than losing weight people doomed to carry extra pounds wouldn't have to feel like outcasts, and would probably be more likely to pursue the correct goal. Instead, most people here seem to think it's okay to berate strangers about their weight. Let them talk to their doctor. If their doctor is good with it, you probably should be too.

@scannex Dude... are you really citing a marketing campaign for weight loss pushers? I bet you I could find data that shows the effectiveness of penis enhancement pills too. If you took a few you might find you like 'em thick ;-). Try some primary literature, and I'll respond in kind.

Try to refute this claim: "Overweight or mildly obese individuals with otherwise normal bio-markers show no decrease in life expectancy from normal."

If you can't, then tell me why it is okay to berate someone about their weight knowing nothing about their health overall?