The essential fact of weight gain or loss is that fat (triglycerides, TGs) stored in fat cells (adipocytes) is made from glycerol (from glucose) and fatty acids (from the blood or recycled from previously stored fat droplets.) Adipocytes must import glucose to make glycerol and TGs.
Glucose Is a Carbohydrate
Glucose is a sugar or carbohydrate. Once again the word tells the story, i.e. carbohydrates consist of carbons that each have a hydrogen, -H, and a hydroxyl -OH attached. Since each glucose has six carbons, then it can be roughly approximated as (H-C-OH)6. This is convenient notation, because this lets glycerol be considered as a three carbon sugar, i.e. (H-C-OH)3.Glycolysis Can Convert Glucose into Two Glycerols
The central metabolism of all cells is called glycolysis, literally breaking glucose. The products of glycolysis are usually high energy electrons (carried by NADH), two pyruvates and ATP (chemical energy). Active cells with access to oxygen can use their mitochondria to accept the high energy electrons and pyruvate, and generate lots of ATP and CO2. Fat cells can bring in glucose by glucose transporters, make glycerol instead of some of the pyruvate and use the rest of the pyruvate by mitochondria to make fatty acids (instead of ATP.)
Fats Have Three Fatty Acids Attached to Glycerol: Triglycerides
Fats, triglycerides, are made in a series of biochemical reactions catalyzed by enzymes. The enzymes first make glycerol phosphate from glycerol and NADH, from glycolysis. Then the fatty acids are attached. The fatty acids can come from three sources: from glycolytic pyruvate, from fatty acids offloaded from the blood stream and from constantly recycled stored fat. Regardless of the source of fatty acid, new glycerol phosphate is needed for TG production in fat cells
Insulin Is Required for Glucose to Enter Adipocytes
Glucose is transported into adipocytes by specialized proteins embedded in their cytoplasmic membranes. A few glucose transporters are always present to supply enough materials and energy for basic maintenance of the adipocytes. Even with very high blood sugar (glucose), the glucose uptake of the adipocytes will not be increased without an increase in the number of glucose transporters in the cytoplasmic membrane. Insulin released into the blood by the pancreas in response to an increase in blood sugar, stimulates the adipocytes to introduce more glucose transporters into their membranes and glucose is actively transported into the adipocytes. The adipocytes then convert the glucose into glycerol, fatty acids and ultimately stored fat.
Without High Blood Sugar and Insulin, Adipocytes Lose Fat
Fatty acids in adipocytes are constantly be converted to fats and then released from storage as they are enzymatically removed from the fats to reappear as free fatty acids. As a consequence, the absence of extra glucose in the adipocytes will mean a shortage of glycerol and a net accumulation of free fatty acids from stored fats. Excess fatty acids will mean that fatty acids will be removed from rather than deposited in adipocytes.
Weight Gain Occurs with High Blood Sugar Regardless of Fats Eaten
Fat will be produced in adipocytes if there is high blood sugar and insulin production, because the fat already stored in the adipocytes will be recycled into fat, any fat in the diet will be converted into stored fat and glucose transported into adipocytes will be converted into fat. In addition, protein in the diet and potentially in muscle, will also be converted into stored fat.
Weight Loss Occurs with Low Carbohydrate Diets Regardless of Fats Eaten
Fats that are eaten without sufficient carbohydrates to cause a rise in blood insulin, are metabolized for energy in liver and muscle. Excess fat ends up being secreted into the gut by the gall bladder and lost as feces. Type I diabetics without insulin cannot get enough glucose into their cells to make fat and cannot gain weight without insulin. The amount of glucose, as simple carbohydrates (sugar or starch), needed to raise blood sugar to trigger a rise in insulin production is typically 30 to 50 grams per meal. Hunger, a response to a drop in blood sugar, prior to the next meal is a typical indication of insulin production and fat storage.
28 comments:
This is suggesting that someone with a low intake of sugary/starchy carbohydrates can lose weight/bodyfat regardless of dietary fat intake i.e. Calories don't count.
Doesn't Acylation Stimulating Protein result in the storage in adipocytes of serum TriAcylGlycerols (TAGs) derived from dietary fats?
Some serum insulin is necessary to allow serum TAGs to enter adipocytes but basal levels are sufficient.
People with untreated type 1 diabetes don't have enough serum insulin so they can't store serum TAGs & glucose resulting in extremely high levels of serum TAGs & glucose (also ketones, as ketogenesis runs unchecked in the absence of insulin).
Nige,
It is great to hear from you. I hope all is OK?
My claims are provocative and based on a major "if". The big question is whether cytoplasmic levels of glucose in adipocytes are low enough to limit acylation (fatty acid loading) of glycerol and thereby TAG synthesis. If that is the case, then low, but functional blood sugar should produce a net production, rather than synthesis of fatty acids in adipocytes.
My contention is that serum TAG never enter adipocytes, only the fatty acids enter. This produces a requirement for glycerol production from glycolysis and acylation to produce storable TAGs.
ASP will be stimulated by dietary TAGs, but I contend that the TAGs will not be stored in the adipocytes, because the ASP will not produce an increase in the required cellular glucose level.
Your assessment of type 1 diabetics indicates that they should produce high levels of ASP, but even with elevated serum TAGs and glucose, they fail to store TAGs in adipocytes.
If you read Bill's comments on my previous post on diet, you will find that he eats a liter a week of olive oil and still fails to gain weight eating a varied diet, but only 50 gm/d of rice as carbs.
I think that my position is extreme and your low carb diets are more reasonable, but I still think that the basic principles are sound. What is shakiest is the transport of lipids in serum, into cells and within the cytoplasm. Triglycerides should stick in the lipid bilayer and not move across membranes. I think that TAGs don't transit membranes and only fatty acids do, via transport proteins. (Same for steroids and alkaloids.)
Thanks for your comments and I appreciate your attempts to educate me in this area.
Art
Your view certainly is provocative! In fact, it's one of the few things that I couldn't agree with when I read Taubes' GCBC.
My experience certainly contradicts this theory. I got gained lots of fat while being on paleo plus dairy and not having more than 40 g of carbs per day. As you know, I suffer from inflammation and maybe this changes the rules...
Then there are the famous plateaus experienced by dieters following Atkins or whatever low carb diet. It could be their diets are so loaded with processed foods that somehow this ends up disturbing an otherwise healthy metabolism. Or that they are simply non compliant and sneak out carbs.
Great post as usual :)
Hi Art. Mum's still deteriorating and I've been feeling depressed which is why I've hardly posted recently.
I gather that TAGs are split into glycerol & fatty acids (FAs) by lipoprotein lipase (which requires some insulin to work) so that FAs can enter adipocytes. The question is, how does glycerol enter/exit adipocytes? My textbook on metabolic processes is not helpful and diagrams show glycerol (also ketones & FAs) passing through cell membranes without showing how.
RE: Bill's diet. I would guess that ~5lb of the 15lb that he lost was water weight due to depletion of muscle glycogen. Ketogenic diets suppress appetite compared to higher-carb diets so it's possible that Bill isn't eating as many kcals each day as before, despite the 8,000kcals/week from EVOO. I can't explain Bill's failure to gain weight when he eats more.
Angela N,
I must confess that my own experience with a low carb diet is rather extreme. Let me give you an example from yesterday -- The raspberry shortbread tart.
It started with the raspberry patch. I like to sit under the redbud tree next to the raspberry patch to read. It gets hot here in Southwest Idaho during the summer, so I run sprinklers in the early morning and after my chair dries (20 % humidity -- high desert), it is deliciously cool for an hour.
So I stare at the ripening raspberries. Unfortunately it is a thick patch and the really tantalizing berries are in the middle, on the old canes. I lose patience, and prune out a path through the non-producing new canes and expose bunches of ripe raspberries.
I then alert my wife to the easy pickings -- she loves to pick berries, if she doesn't have to wade into prickly bushes. We end up with a pint of ripe, tender berries, that brings up visions of tarts.
The internet overflows with recipes and a thin shortbread crust is baking and the berries are waiting. After the crust has cooled, the berried are studded thickly across the surface and the juices of the berries start to stain the crust.
That is the problem with starch. Just a thin slice caused a noticeable shift in my metabolism and my carb lust. Within an hour of my first exposure to the palate satisfying crust, I was hungry, with a growling stomach. This is very unusual, because I typically am never hungry, even when I skip meals. For the rest of the day, I was chasing my stomach and craving carbs that I normally ignore.
Carbs bring out the Jekyll in me.
Thanks for the post.
Art
Nige,
Wikipedia to the rescue (as you always recommend.)
I am trying to get my head around the biochem of chylomicron, VLDL, LDL, HDL, lipoproteins, LPL receptors, lipases, etc.
I think that the critical parts for this discussion are LDL attachment to adipocytes by LDL receptors (they use heparan, by the way), endocytosis, release of fatty acids into lysosomal membranes, and the opposite path of the fatty acids back out. The process isn't reversible, because HDL removal of FAs seems to be pecking at the cytoplasmic membrane and not secretion.
Glycerol isn't transported into adipocytes, it is made from glucose in the adipocytes as a branch of glycolysis. That is my main point of constant low blood sugar -- the source of glycerol is cut off and TAGs can't be made in the adipocytes. The net result of glucose/glycerol restriction is HDL removal of the excess FAs from the adipocytes.
Glycogen depletion is an interesting point. I wonder if glycogen-derived glucose could be sufficient as a source for fat storage? The result for some people is that they could periodically build up their glycogen with a carb binge and use that glucose to continue to store fat even on a low carb diet.
Depression feeds on inflammation, so please eat smart to help your mood. Keep blogging. There are a lot of people who need your diet wisdom.
Art
Tarts are indeed the summit of a slippery slope. At least if you need to pick more berries and bake again if you want too much more, vs. jumping in the car and going shopping for a prepared tart. That's my strategy with ice cream, a tempting but somewhat less diet-busting treat than tarts (for me). I indulge in ice cream if I make it (high in cream and egg yolks, fairly low in sugar compared to commercial ice cream). I can't make more until the freezer bowl has been thawed, cleaned, and refrozen at least 24 hours (realistically at least 48 hours later). So that precludes form over-indulging in ice cream (and I've never actually made it that frequently, plus there is always someone else around to make sure I can't eat the entire batch myself ;-). Buying ice cream just leads to too much carb indulgence, so I rarely buy it (unless I'm in Italy or someplace with fantastic high quality gelato/ice cream).
I've been eating low carb for over 5 years now, initially to lose the 20 pounds I gained after buying a bread machine, but now it's to maintain my weight and to maintain normal steady blood glucose levels (IGT). I didn't follow any particular LC plan, I read up on them all, and just restricted or avoided most high carb foods, made sure I was consuming adequate protein, and raised my natural fat intake (mostly saturated). Enough natural fat seems to be key to not only weight maintenance but also energy levels and "oomph", otherwise I become lethargic.
Over the last 3 years I dropped the use of quite a lot of packaged and prepared foods (esp the LC processed foods) and transitioned to sourcing my family's meat, eggs, produce, dairy, EVOO, and nuts direct from ranchers, farmers, etc.
I always wonder about those famous "Atkin's stalls", because most of the people I observe who claim to follow Atkins, either only "cycle on Atkins" for a time or they basically eat a constant LC diet of processed manufactured foods, not naturally low carb real foods. The carb counts *are* low, but so is the nutrient quality and quantity generally. Perhaps the cells are still "starving" for the nutrients they need, so they hold on to the fat anyway.
Anna,
Thanks for stopping by.
I guess that obesity should be considered malnutrition. I think that obesity comes from dietary ignorance (which foods have carbs, protein, fat, etc.?) and an abundance of unhealthy foods.
I am shocked at the number of professional meetings that I have attended where the catered breakfasts have only starch and no protein choices. The closest they come is with fruit that high in fructose.
Thanks for the comments.
Art
Gary Taubes Dartmouth lecture
Using the THUMBS tab you can move directly to slides 41~50 to listen to the Taubes version as referred to by Angela N.
Slide 47 is where he discusses the critical role of glyerol-3-phosphate and it's interesting to hear his very last comment at the very end of this particular slide.
May I use your blog to pass on my best regards to Nige.
I know it's too late to help in your mother's current situation but the information people like you and Art of course, provide will ultimately help prevent others ending up with conditions like Alzheimer's.
I know it seems like a thankless task, but your ability to explain the science, allows people like me to understand it better and thus the message spreads slowly but surely.
Ted,
Thanks for providing the link to Taubes' lecture. The data on blood transport has been greatly refined since the 70's (LDL, HDL, etct.), but the major point of fatty acid, rather than TAG, import is still valid.
Thanks for the encouragement. I must indicate that Nige brought your vitamin D article to my attention and it has changed my outlook on inflammation. Vitamin D deficiency and leptin levels may be a major part of inflammation and obesity.
Thank again for your comments.
Taubes Lecture
Note that at the end of the lecture, he is asked if gut flora have any impact on obesity. Taubes answers that the gut flora would only make a difference, if they altered adipocyte metabolism. He was skeptical and thought it was another fake.
I think that the gut flora control the immune system and thereby alter adipocyte metabolism. This would explain the fecal transplant experiments between lean and obese subjects -- lean with obese flora gain weight on the same diet.
We know little about communication between gut and gut flora. What we do know is that hospital residence dramatically alters gut flora and increases inflammation. Does inflammation predispose to obesity? I think so.
'Carb lust...'
*haa*
I'm going to steal that honey is that ok? Honey... that gives me carb lust. I had to stop that in my coffee...
-G
That Gary Taubes lecture took a while to get to the point, but it was interesting. I guess I'll finally have to buy his Good Calories, Bad Calories book.
Thank you Ted.
There are more questions than answers. How does ASP stimulate the synthesis of TAGs within adipocytes if the supply of glycerol 3 phosphate there is limited? Does anyone know any experts on metabolic pathways who might be able to help?
With an oral fat load, where do serum TAGs go if there is no significant insulin increase? See Fig 1A in Metabolic response of Acylation Stimulating Protein to an oral fat load. I have difficulty believing that significant amounts of TAGs end up down the toilet, as significant amounts of fats that aren't absorbed during digestion cause greasy diarrhoea (as some people who take Xenical, a lipase inhibitor, discover).
In the real world, people on low-carb/paleo/keto diets don't eat meals consisting of fats and nothing else. Meals tend to be proteins+fats+fibrous veggies. Proteins produce an insulin response as per Insulin Index and fats increase the insulin response as per Fig 1B of The Degree of Fat Saturation Does Not Alter Glycemic, Insulinemic or Satiety Responses to a Starchy Staple in Healthy Men.
I'm not suggesting that low-carb/paleo/keto diets aren't effective for bodyfat loss, as they clearly are. It's only the issue of eating unlimited amounts of fat not making you fat that I disagree with.
Nigel,
I consider myself a technician in life, and not a scientist. In my work, and now with my diet/body, I select from the latest tools and knowledge available, and apply, using my judgement (normally lateral/unconventional thinking) to obtain results.
I am seeing a dietician at the hospital tomorrow, it will be interesting to discuss my diet, with the high olive oil consumption with her, and her conclusions. Maybe I can ask for a stool analysis....
My stools are usually soft and smelly! Considering the half bulb of garlic, half an onion, scotch bonnet chilli and thumb size fresh ginger, per portion, this would be expected. Normally passed 6-8 hours after eating.
I do not cheat, and apart from the sugar in 90% cocoa chocolate, 30gm/d, I do not eat sugar and definitely no grains or legumes. So that leaves 50gm/d of basmati rice.
Hope this gives you more to chew on. (pardon the pun!)
Just a thought. With my diet I always try to minimise omega 6 fatty acids and optimise omega 3. I use extra virgin olive oil, because I have read that evoo does not affect the omega 3/6 balance of the diet. I'll dig out the link....
Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases
It's not very often that papers have me laughing out loud but I really enjoyed reading the concluding remarks here.
I'd be interested in hearing Art's reaction to this novel approach to consideration of the idea that the role of poorly liganded iron has been rather underappreciated in the past, and that in combination with peroxide and superoxide its activity underpins the behaviour of a great many physiological processes that degrade over time.
Where does the fat go in a high fat low carb diet without weight gain?
High fats stimulates bile production, fat uptake, TAG conversion to FA in LDL, FA offloaded into lysosomes of adipocytes.
FA in adipocytes from cycling of stored TAG, imported FA from LDL. Excess FA leaves via cytomembranes by HDL to liver to bile to toilet. The adipocyte FA pools must be saturated with low TAG accumulation, otherwise there would be body fat.
The ASP is increasing insulin and increasing FA offloading into adipocytes, but the low blood glucose prevents TAG production in adipocytes, except for the two hours after carb consumption. When the blood sugar drops, the carbs are pulled back out of the adipocytes, because the TAGs are continuously cycling back to FAs and the glycerol eventually gets converted to more FA.
If there is an average low blood sugar, then adipocytes will empty. If there is high blood sugar, but not insulin (diabetic), then there is the same result of empty adipocytes.
The question may be what happens to HDL that is loaded with FAs taken from adipocytes, e.g. during fasting? What if the liver is already saturated with FA? Does this result in excess bile containing fatty acids as emollients? Fatty acids are soap and would give different stools than TAGs. The stools should float and disrupt surface tension.
Hi Dr A,
I guess everyone is an experiment of one. I tried the Atkins a few years ago. I would test urine and could track ketonurea. I never found lipids (floaties) in the toilet. I gave it up when my cholesterol went to 300. Now on the Zone I see the cholesterol is coming down. One thing I found was the ratio of TC, LDL and HDL were fixed. They ratios didn't change when cholesterol was 300 vs 160.
kevin
Cristian,
Another great find. The idea that mitochondrial superoxide is a trigger for insulin resistance, is a nice unifying hypothesis. It explains a lot.
Thanks for your insightful contributions.
Now that my brain is working properly again, I would like to propose a theory which explains how fat cells can acquire glucose (& thus correct a deficiency in glycerol-3-phosphate) even when serum insulin level is basal.
Consider muscle cells undergoing anaerobic activity:-
Anaerobic activity is very inefficient and uses pyruvate at a very rapid rate. A deficiency in pyruvate up-regulates all of the up-stream processes, including GLUT-4 transporters so as to maximise pyruvate production.
This explains why resistance training with weights greatly increases muscular insulin sensitivity and why resistance training with weights when depleted of muscle glycogen can cause precipitous drops in blood glucose level.
Ditto for glycerol-3-phosphate in fat cells. In this case, blood glucose level is maintained by the liver, which converts the glycerol backbone of triacylglycerols (fats) into glucose.
Cheers, Nige.
Nigel,
This suggests that the fatty acids would be released into blood and presumably the fatty acids would be bound to carrier proteins. This could displace or compete with steroids for carriers. It is interesting to me that the ends of several of the collagens and some of the other typical extracellular proteins, e.g. laminin, have the squished jelly doughnut configuration capable of carrying steroids/lipids. Perhaps excess fatty acids changes connective tissue structure/function.
Thanks for hanging around.
@Nige
Have you seen this:
http://www.rawpaleoforum.com/journals/lex%27s-journal/msg1075/#msg1075
"Eating Carbs creates insulin - insulin metabolizes glucose - alpha-G-phospahte is created - liver uses a-g-p to create triglicerides - triglicerides are then moved into fat cells. Bottom line no a-g-p no fat can be stored, at least that's the theory.
Taubes also stated that 58% of protein can be converted to glucose, but didn't say how or when this would happen. If this is true, then too much protein in the diet could cause a rise in insulin thereby creating a-g-p and causing fat storage.
My experience was that when I started eating this way I started with a higher fat content in my meat. Initially my weight dropped to about 150 lbs but then I got lazy and stopped adding the fat to my mix. Over several months my weight increased to 160 and then stabilized at that level.
I decided to test Taubes theory. If he is correct, since I don't eat any carbs my only source for glucose is from protein. If I reduce the protein and raise the fat to bring the calories back up, then less glucose would be produced and I should again lose weight even though calories stay the same. Less protein means less glucose created, hence less a-g-p all leading to less fat.
Still early yet but this seems to be working just as Taubes expected. My average blood glucose had been reduce by about 20 points since I made the change 2 weeks ago. I've lost 2 lbs in 14 days. Ketones went from less than Trace to Moderate which shows that body fat is being consumed. I have no idea how far this will go but intend to stick with it for several months at least and maybe forever.
There is a minimum amount of protein that the body will always need and I can't go below that amount or my health will suffer. This amount is between .8g and 1.4g of protein per KG of lean body weight. for me this is about 85g protein per day. This will produce about 50g of glucose and my final stable weight should be based on this amount.
Part of what was not clear in Taubes lecture, and no one else seemed to know, was if some portion of all protein eaten is converted to glucose or if this only happens in a metabolic emergency. The infamous “Bear” (Stanley Owsley) said this conversion only happened in metabolic emergency. I’m finding that this is not true.
What I'm finding is that all protein eaten is converted to glucose at the rate of about 58%. This was demonstrated to me by the drop in blood glucose levels when I changed my diet from 32% protein to less than 20% protein.
My original protein consumption was about 150g/day. This converted to 87g of glucose and you could see my blood glucose level rise about 25 points over a three hour period and then it would decline to an average resting value over the next 18 hours or so before finally dropping to the original starting level a couple of hours before I ate my next daily meal.
When I cut the protein to 90g/day (I raised fat to keep calories the same) there is 52g glucose created and my blood glucose levels only rise 15 points before dropping back to the average resting value.
What is interesting is that the drop in protein from 150g/day to 90g/day is a 40% drop. The "calculated" drop in glucose manufactured from protein from 87g to 52g is a 40% drop. The measured change in the rise of blood glucose directly after eating a meal from 25 points to 15 points is also a 40% drop - so all these numbers track exactly."
Patrik said...
@Nige
Have you seen this:
http://www.rawpaleoforum.com/journals/lex%27s-journal/msg1075/#msg1075
"Eating Carbs creates insulin - insulin metabolizes glucose - alpha-G-phospahte is created - liver uses a-g-p to create triglicerides - triglicerides are then moved into fat cells. Bottom line no a-g-p no fat can be stored, at least that's the theory."
I have, now! I totally agree with "no a-g-p no fat can be stored". My theory suggests that a-g-p availability is not limited by serum insulin (provided that there is some i.e. the person doesn't have untreated type 1 diabetes).
I've left a comment on Can protein turn into fat? but it hasn't passed moderation yet. The second question links to here. The first question is about the thermogenic effect of dietary fat. IIRC:-
It's generally believed that dietary fat has virtually zero thermogenic effect. Is it possible that the thermogenic effect varies with a) chain length & degree of saturation of the FAs in the fat (i.e. the SCFAs in butter & coconut oil are thermogenic but LCFAs aren't) and b) the subjects' insulin sensitivity? This would explain why some people lose loads of weight on HFLC diets and others gain.
P.S. I converted your url into a link using _a href="url">Text_/a> where _ is the < symbol.
Patrik also said...
@Nige
"I decided to test Taubes theory. If he is correct, since I don't eat any carbs my only source for glucose is from protein. If I reduce the protein and raise the fat to bring the calories back up, then less glucose would be produced and I should again lose weight even though calories stay the same. Less protein means less glucose created, hence less a-g-p all leading to less fat.
Still early yet but this seems to be working just as Taubes expected. My average blood glucose had been reduce by about 20 points since I made the change 2 weeks ago. I've lost 2 lbs in 14 days. Ketones went from less than Trace to Moderate which shows that body fat is being consumed."
1) How did you measure your caloric intake?
2) Do you know how much of the 2 lbs was glycogen+water and how much was body fat? Ketones in the blood & urine shows that fat is being burned, but you don't know how much of it is dietary fat & how much is body fat.
Nige.
Dr Ayers and everyone - very great article and comments - I always learn so much here - I am trying (again) to follow a proper low-carb diet after see-sawing back and forth with low-fat (gasp) but at least gluten-free, but too much fructose ...
I do have a question, though - Now I am eating greek-style yogurt, perhaps too much (1-2 cups per day) and cheese - and I am gaining body fat fairly quickly - too much carbohydrate do you think ??
thanks very nuch :)
Elizabeth,
Yogurt is great, but in moderation. A high fat, 30% protein and veggies diet is fairly tolerant to extra fat, but there is a limit. The same diet with more than 20 gm carbs per meal can put on fat quickly.
Eliminate the fructose. This is a problem for any diet and changes your metabolism.
I think that you can lose those pounds by cutting back on the yogurt and eating less carbs, or by using more portion control. Exercise can improve health, but you just can't compensate for extra calorie consumption by exercising to use up calories. One cookie equals a very long walk.
Dr. Art Ayers,
Stephan Guyenet,the owner of Whole Health Source blog, said in his artcile" The Carbohydrate Hypothesis of Obesity: a Critical Examination" that Taubes's claim regarding the role of insulin on obesity is wrong. Eating carbs that spikes insulin level does not make people fat.
What's your though on this?
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