For some weird reason I decided to read Durianrider's blog today. I'm sure you can find it. Not only is it unusual for me to read this whacko's scribes, but I was really busy today at work. I'm glad I did though.
He wrote about forms of of mental disorders, mainly three forms of dimentia, according to his definition, alzheimers, mad cow disease, and AIDS. I guess he couldn't include psychosis
He has a strange way of twisting logic to suit his needs. If you don't know him, he needs to mutilate things like logical thinking and scientific methods. Of course he blames all three of these diseases on meat consumption.
Perhaps his silliest case is AIDS: Scientists believe that the origins of AIDS also are related to the consumption of meat, and specifically bushmeat in Africa. Really? I checked it out. The first site I found was The Origin of AIDS and HIV May Not Be What You Have Learned , and it is a very good looking site, says this: Most people believe that the origin of HIV, the AIDS virus, derives from some natural evolutionary event. Key among these HIV origin theories is the so called "cut hunter theory" in which a human, allegedly African native, received a bloody wound or infected splash while preparing a chimpanzee carrying a similar virus (i.e., SIVcpz). Most recent research, along with the scientific consensus, holds that the origin of HIV and AIDS could never have happened this way. If you read carefully you'll note that it wasn't blamed on meat consumption. It was blamed on exchange of blood while cleaning a chimpanzee, arguably the closest relative to humans, Case closed? I'm not digging further. But if you can show me some real science linking AIDS to meat consumption, please bring it on!
Next he digs into mad cow disease and alzheimers. First he states Mad cow disease is specifically related to the consumption of meat. Related is a rather nebulous word. Does he mean cows ate meat? Cows have been fed meat at one time. Should cow eat cow? It was banned because it supposedly caused this condition. Or does he mean we get it from eating cows? I don't know if that's been proven, but I'll give it to him. But I wonder if he asked why cows get mad cow disease. Wikipedia, the Olde Faithful of blogging argument support says this. Bovine spongiform encephalopathy - Wikipedia, the free encyclopedia It is notable that there are no cases reported in Argentina, Australia, Brazil, New Zealand, Uruguay, and Vanuatu where cattle are mainly fed outside on grass pasture and, mostly in Australia, non-grass feeding is done only as a final finishing. Interesting! What John giveth, Wikipedia taketh away.
The limited evidence I've discovered on the next points seems to confirm my preference for the cause: grains!
He then discusses alzheimers and how his favorite veggie doctor thinks it's caused by eating meat based on some nebulous -- I hate this word, but this is the way buddy writes -- associations. He writes that amyloid proteins are associated with alzheimers. Yup, I think it is. He says it's also associated with type 2 diabetes. Yup again. But so what? Any decent logician knows that associations do not indicate cause. Enough of that. You've heard it before. He goes on to say several wonky things:
He goes on about causes and even slips in that healthy people not only don't eat meat, but they also don't eat clarified sugars, bleached grains, and artificial chemicals. So which is it, the meat or these other nasties? Logic. He has none.
But the Amyloid thing is what turned my crank. I'd never really paid any attention to them, you know, this nasty association business. I tend to simply shrug those finding off. I was now curious about them, so I did some reading. I couldn't find any causes of amyloid buildup anywhere, but this site was very interesting. It describes how these things might cause type 2 diabetes:
AMYLOID PROTEIN–A CAUSE OF DIABETES / Diabetes / Dr. Pinna
It found that a type of immune cell called a macrophage, whose normal role is to get rid of debris in the cell, reacted abnormally when it ingested amyloid. It triggered activity in other cells nicknamed angry macrophages, which in turn released proteins that cause inflammation. The inflammation then destroys the vital beta cells, and the ability to produce insulin is reduced.
If you're on the same page as I am, you recognize macrophages from atherosclerosis development. Could these amyloids also be at the root of atherosclerosis? I don't know, but I'll be watching.
As I leave I'm overcome with temptation. I need to leave you with a Durianriderism logic argument:
Dr. Pinna says:Take lots of Vitamin B complex. It seems to reduce amyloid.
B Complex reduces amyloid? Where does B complex come from. Can you say MEAT?
P.S. Here are a couple more articles I read today suggesting meat and fat are not to blame for mental disorders.
Evolutionary Psychiatry: Do Carbs Make You Crazy?
There is tension in the world of cholesterol. Those of us eating high saturated fat,low carbohydrate diets are claiming that this is much better for heart disease prevention because we increase the size of our LDL particles. The problem seems to be though, that the medical establisment can't take their sights off of the LDL value in our standard lipid measurements. I think we can all agree that the LDL value alone is a lousy predictor of heart diease. Even teh staunchest cardiologists admit this. However, it's the best we have. *gawd*
The problem is these policy setting scientists that have listened to their cheque-writers (For you Americans, a cheque is a check. If you can't handle such a change, you shouldn't be reading my blog!). They have listened so hard, they forgot to follow teh real science. Now that science is catching up to them. In my opinion, the stage is almost set for some class action lawsuits against the NHLBI and USDA for setting policy according to paycheques and not science. The key point I want to make clearis they are very likely looking for a way out, a compromise if you will.
I'm hearing some rumblings about a new measurement. It's not that new, but it hasn't been used much. It's not been set in policy or even discussed by teh ATP in their timely seven year reports. Good God, the number one killer in America only gets discussed every seven years. Another slant against them if a law suit gets launched. Anyway, this new measurement amazing keeps the old LDL value in play and also seems to accomodate the new breed of lipidologists like myself. It's called non-HDL cholesterol.
NHC? Is that it? Yup, that's it. I do not know if the VLDL value nees to be added into the total value. It's the sum of all cholesterol or APO-B particles. The theory says that APO-B is actually what's dangerous, so we should measure it all. Correct me if I'm wrong, but I always thought HDL used the same APO-B as LDL, the APO-B 100 protein. Basically what they are saying is both LDL and VLDL are atherogenic, VLDL being the lipoprotein not currently measured. Amazingly it seems that those persons with LDL that experience heart atacks do in fact have high VLDL numbers, so this new capture may in fact be much more relevant. It also opens up the door for doctors to accept those up us on HFLC diets whose LDL value increases. Maybe. Doctors, just like my fellow Americans, do not like to change. [sorry, but politics is getting to me lately]. I hope this accomodates the new LDL size way of thinking. I really do.
It should fit my way of thinking, that LDL size is the cause of modern heart disease, and that LDL size is based on triglyceride levels. Triglyerides are caried by VLDL aprticles. Therefore, high trigs means high VLDL which means high NHC. Win, win, win!
So scientists now have a compromise which lets them off the hook for hundreds of millions of early deaths, rampant obesity, and the entire host of western diseases. Wow. We new self-proclaimed [really, we know squat] lipidologists are acknowledged, and most importantly it opens teh door to change our food guidelines and systems. It's not a wholesale admittal of wrong advice but a step towards better advice.
I still hope somebody sues their butts!
Thanks for visiting my blog post, I am Sharon D. Jones.
I was diagnosed in May 2006 with diabetes with a HbA1c of 9.8%, from oct 2006 I was placed on insulin therapy to control blood sugars that did not respond to oral medications.
I enjoyed excellent control whilst on insulin therapy but I knew that one day I would challenge the conventional view that diabetes is irreversible.
In July 2009 I started out on an experiment that would change my life, I adopted the alkaline diet and within five short weeks my insulin requirements dropped from 23 units per day to zero!
‘Alkalise Me’ is the book I wrote about my experiences on the alkaline diet during those first crucial weeks and first tentative steps into diet control after being insulin dependent.
It was written in the hope that others may be inspired to do the same.
Sharon D. Jones
Alkalise Me is available in Paperback and Kindle from amazon and major book stores.
Kindle: ASIN: B0051UMG5G
In the last few days there has been a backlash against diabetic educators (DE's), particularly one named Hope Warsaw, or affectionately called "High Carb Hope" by some of us more vocal anti-DE writers. I won't go into the details of what she wrote to raise the ire of the Paleo community, but here's some recent blogs.
Livin' La Vida Low-Carb
Healthy Low Carb Living
and a more generic The Poor Diabetic
I read her article, got angry, posted a reply, and moved on. I am upset, but I know there's nothing I can say or write to change her mind. It doesn't matter to her that I've dropped thirty pounds, that my HDL is as high as my LDL, which has gone up, or my triglycerides are as low as triglycerides can get at 42. It doesn't matter that my proliferative retinopathy has fully stabilized, that my sexual functioning has improved, my aerobic performance has improved, or that there's absolutely no signs of atherosclerisis in my eyes. She believes I'm killing myself with a fad diet, but why does she believe this?
One reason she believes is because she sees her recommendations working, and studies show it does. Her Mediterranean diet does work better than the standard American diet or SAD. People who follow her advice do better. If you are one of the 90% of diabetics who fail to achieve good control, and your diet, well, if your diet sucks, then follow her advice. It will be an improvement. It's not the best plan. A primal diet is best. Eat 60% fat -- mostly saturated -- 30% protein, and 10% carbs. Make sure all this food is as natural as possible.
The main reason she believes though is because she trusts her own guidance. She was educated to believe what she believes, and the official nutrition and health comminities all push the same message as she spouts. She's less than the tip of a mammoth iceberg.
I want to target the base of this mess, the root of all this diet nonsense we've been fed the last 34 years. I want to target the National Heart Lung and Blood Institute's Adult Treatment Panel. This panel of scientists sets cholesterol treatment policy for the world, and since heart disease is such a big killer, everybody follows what they say. The USDA food guide, endocrinologists, the American Diabetes Association, the American Heart Association, and every country's equivalents around the globe base their guidance on the ATP's recommendations. They will not change their cholesterol treatment guidelines until the ATP changes their tune.
ATP IV is scheduled to meet later this summer: Background, CVD Risk Reduction, Cholesterol, Hypertension, and Obesity Guidelines, NHLBI I took a look at the panel and searched for the web for anything about them. Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel IV), Expert Panel Memberhip, Health Professionals - NHLBI, NIH I won't post my findings now; because they are on my laptop at work, I think. My cursory assessment goes like this
Low Carb: Daniel Rader, M.D. University of Pennsylvania
Undecided: Ronald M. Krauss, M.D. Children's Hospital Oakland Research Institute and Frank M. Sacks, M.D. Harvard University School of Public Health
High Carb: 13 pawns
Dr. Krauss authored the infamous meta analysis that showed no associations between saturated fat and heart disease. I initially held out some hope for him, but an interview I heard with him on one of the blog-casts told me he is not yet converted. Dr. Sacks has been a hard core anti-fatologist, but he seems to have softened after working with Dr. Krauss. Dr. Rader's comments showed promise, but the rest are all staunch industry backers. Why did I call them this? Take a look at the ATP III conflict of interest. Review this page: ATP III Update 2004--Financial Disclosure, NHLBI, NCEP It is my firm belief that this so-called scientists tow the line. Admitting current guidelines are wrong is the same as cutting off their own money supply. Say cholesterol is not the enemy means Big Pharma won't sell many drugs. If they collapse, their funding collapses.
So do we have hope of breaking these high carb shackles? I don't have much at the moment, not if we all keep attacking the middleman, the diabetic educators. I want to turn our guns on the ATP. I want them to stand up and acknowledge the real science, behave with some scientific integrity, some hypocraticness and make the logical decision to target sugar, not fat and cholesterol.
It's the sugar stupid!
We get fat is because we eat too much, right? That's what our doctors tell us. That's what our dietitians tell us. That's what diet gurus tell us. Weight Watchers and other diets work because we reduce calories. Exercise works because it burns calories.
So why is there an obesity epidemic? Why do 97% of dieters fail?
There is one simple fact that refutes the whole concept of calories in vs. calories out. It's called type 1 diabetes.
We need to review what happens to type 1 diabetics. What, not why.
Our bodies stop making insulin, our tissue -- not all tissue -- cannot ustilize glucose. Our brain, heart, and other organs can, but not much if anything else can. Our food stores, our fat, glycogen, and muscle will be used up and we will die. Correct me if I'm wrong, but we don't actually starve to death. We die from glucose toxicity as the blood glucose levels skyrocket and stay at toxic levels. We can still utilize fats and proteins. The important point for this argument is we will not store fat or glycogen.
Let me repeat this. Without insulin, we will not store fat or glycogen. It doesn't matter how much we eat, it doesn't matter what we eat, eat 100,000 calories a day if you can, we will not store fat or glycogen. Do you understand this point? Storing fat and glycogen is not possible without insulin. If it's merely a case of calories in vs. calories out, how come type 1 diabetes even exists?
Don't brush this off. It's fundamental metabolism. Insulin controls adipose tissue. It's in medical textbooks. If you want to control your weight, the ONLY way to do it is by controlling your insulin levels. Don't make me starve myself to prove this, which I can easily do. Almost all diets are lower carb and therefore lower insulin. If you are losing weight, you are lowering your insulin levels.
Let me repeat this once again for the thick-headed readers: it doesn't matter how much we eat, it doesn't matter what we eat, we will not store fat or glycogen without insulin.
The next time some medical person says you only need to eat less to lose weight, ask them "if that's true, why does type 1 diabetes exists?" It cannot be rationalized. Watch them squirm!
Could have been written by the Rolling Stones: "I Don't Want No Complications"?
I don’t want no complications.
I don’t want no complications.
So I test and I test and I test and I test
I don’t want no, I don’t want no.
When I'm orderin’ my food
and deciding what to eat
well, I’m countin’ carbs more and more
to get some useful information
to help avoid any complication.
I don’t want no, oh no no no.
Hey hey hey, that's what I say.
I don’t want no complications.
I don’t want no complications.
So I test and I test and I test and I test
I don’t want no, I don’t want no.
When I'm watchin' my TV
and that man comes on to tell me
how good my food can be.
Well he’s not talking to me ‘cause he don’t say
How many carbs in that treat.
I don’t want no, oh no no no.
Hey hey hey, that's what I say.
I don’t want no complications,
I don’t want no situations
So I test and I test and I test and I test.
I can't get no, I can't get no.
When I'm ridin' down the street
and I'm doin' this and I'm eatin’ that
and I'm tryin' to score some treat
what tells me baby better pick something else to eat
my meter--I am a control freak.
I don’t want no, oh no no no.
Hey hey hey, that's what I say.
I don’t want no, I don’t want no,
I don’t want no complications
no complications, no complications, no complications.
Over the past 3 months or so I've had great success in eliminating really bad lows. However, in the last two weeks or so I've had three or four really bad hypos and each time I was walking around in very hot, humid weather. Has anyone else noticed this connection?
Some time ago I listened to a podcast with Dr. Rosedale. It was probably one of Jimmy Moore's. He said some interesting things about fat metabolism. His premise was that a healthy person is somebody who burns fat. If your not burning it, you're storing it, including in arteries. It has stuck with me and forms a basis of my eating -- a ketogenic diet.
Recently I found myself thinking about protein metabolism, particularly gluconeogenesis (GNG). We type 1's have runaway GNG due to our absence of the hormone amylin. What got me thinking about this further was a post here (maybe elsewhere) about weight distribution of type 1s. Many say we tend to be skinny and I say otherwise, so I tried to find some evidence online that we are normal. I found a study that said we were nearly normal with the exception that many of us are skinny. Great. Thanks for clarifying.
So there are many skinny type 1's. Why? We generally take more insulin than the normal person; we should all be fatter. What could be going on? My thoughts turned to protein. I don't know any muscular type 1's. I'm not. I can gain muscle; I have. I gain fairly easily in my legs, but my upper body tends to be weak. If I train for six months I can work up to 3x10 120lb bench presses. My 19yr old son can do that much without training. I also lose muscle mass easily. I just started weight training again this week, and I'm starting off at very low weights. 120lb squats should be something I can do on one leg all day long, but it's a struggle at the moment to get 15 reps in.
So I'm guessing that we skinny and muscle-challenged type 1's are fighting GNG as a protein drain. It consumes protein, including our muscles. It seems reasonable to me. But here's a question: what impact does resistance training have on GNG? If I lift heavy weights, will muscle repair override GNG demands? Will I reduce the protein draw? Will my sugar production come down? Will my insulin levels fall? Will I lose fat because of this?
This is my current experiment. Let's see if I leave everything else the same what some intense resistance training will do for me. Starting weight: 225lbs.
Our doctors treat blood pressure (BP) very simply: "take these meds and don't eat salt."
Do doctors really understand the cause of high BP? Do they really know how to treat it? Or are they simply going through the motions, covering their asses just in case we die from it? And by doctors I mean the whole medical community from the Surgeon General down to your lowly ditetitian. The fact that our dietitians are on the bottom of the chain might be a topic for another discussion. Our health depends on nutrition.
So what is high BP and what should we do about it? Let's first discuss conventional wisdom.
High BP is simply high blood pressure. One cause is supposedly that the arteries become stiff and become less flexible. If they can't expand as widely, more pressure builds up. It seems plausible, but does science prove it? This study didn't http://www.ncbi.nlm.nih.gov/pubmed/2632754 This Mayo article suggests stifness results in low diastolic and high systolic pressures: http://articles.sun-sentinel.com/2010-06-22/health/fl-jjps-pressure-0623-20100622_1_blood-pressure-blood-loss-diastolic/2 I suppose if they can't expand, tehy can't contract. This statement from the last site is interesting. Atherosclerosis — a condition in which fat (plaque) builds up in and on artery walls — can stiffen blood vessels and have the same effect on blood pressure. A little logic tells us that if the first study is true, that stiffness doesn't really affect BP, then this last sentence is wrong. I suspect it is very wrong.
Most practitioners promote the idea that sodium in our diets is responsible for high BP. High sodium causes us to retain water which raises our BP, another plausible idea that's pushed on us hard. It makes sense except for a couple of things. First, there's very little evidence it works. Find it for me please! Second, it shoudn't work. Huh, you ask.
Our sodium levels are tightly controlled. If they weren't, we'd be dead. Too little or too much sodium will kill you. Exactly how much is not clear, but that's not the main point. The main point is that if you eat too much, you pee out the excess, and if you don't eat enough, you will retain it. Homeostasis.
Another idea is excess weight can cause it. "Lose ten percent of your body weight, and your BP will come down." I was recently told this in a diabetes education class.
My friend Dan weighs over 400 pounds. He can't be wighed at the doctors' office. They have to weigh him at truck stops. He has high blood pressure. We discussed his history: he gained about 40 pounds the previous year and his blood pressure was high before and was high then. I got him to try eating like me. His sinsulin dropped dramatically, he lost 40 pounds, and his BP was almost normal. Unfortunately he hasn`t stuck with it. He thinks boxes of Oreos are okay to eat. But it was interesting to see his BP results. At 360 pounds on the way up, he has high BP, but on the way down, he has more normal BP. It`s not the weight. In my case, I`m still overweight by some 40lbs. Yesterday I tested at 105é59 after a day in the garden. I`m pretty sure it`s not the weight causing high BP.
I highly suspect -- of course I don't really know these things -- that atheroclerosis, excess weight, diabetes, and high BP are symptoms of the same cause. We discuss this cause all the time. I think it causes most of our diabetes troubles and probably most of our western diseases. I think our medical community is guilty of making false assumptions about cause and effect. Of course I'm talking about high sugar consumption. Sugar (all carbs and half of protein) consumption causes higher insulin levels. Gary Taubes asserts that high insulin causes the kidneys to retain salt. When you retain more salt, you retain more water and your BP rises. You will see a criticism of the Atkins Diet: "It`s all water loss. It`s not really fat loss, and it`s not healthy!" But your BP dropped. Hello? Your BP dropped!
Cut the sugar, elimate atherogenic LDLs, lose the weight, lower your BP, become more active as you stop feeding your fat, and basically get healthy.
i can still remember how it felt when the ER doctor told me i was diabetic... it was march 25th, 1992 and just after 11am... i had, what i thought, was a simple yeast infection, though i was 15, i kinda hoped it wasn't that cuz i had always believed what one of my sisters said about yeast infections (you get them if you're dirty and don't clean properly)... so i was secretly wishing it wasn't that... that it was anything but that... not knowing what the 'anything' could be...
the doctor took a stick test and i was at 34.7 (625)... when i was told it was diabetic and because of my level, i was type 1, which was called "insulinodependant diabetic"... long name but the insulin thing was lost on me... the doctor came out of his office and started getting physically mad with my GP, who was in the same medical clinic... turns out my levels when i had T4 blood tests for my hypothyroidism were elevated to the point of being in the teens (180 to 300)... and i was never told that i was diabetic... the endo who was treating me for my thyroid kept saying my blood sugars were slightly up because i was overweight for my age...
my GP wasn't responsible for not telling me, but he was accountable for never noticing the high levels... but i never complained to anyone, nor did i sue or anything of the sort... i did, however, stop going to that endo...
anywho... i was sent to a local hospital and spent the better part of the first day learning the terms, injection styles, reasons for, complications of, and, oddly enough, i was made to smell different levels of gangrene, from beginning of to complete necrosis...
my two older sisters were at home (it was a wednesday) by the time my parents left the hospital... i didn't see anyone until the day after because by the time my parents got home and told my sisters and had something to eat, it was past visiting hours and i was on the peds floor since i was 15, and i felt so alone... all i had with me was my sony walkman...
the batteries were getting low so i listened to the radio until i fell asleep... most of the stations where doing elton john songs because it was his 45th birthday... i was so depressed at the time, that listening to his songs helped me thru the first day...
i also snapped out of the blues because there was a little 4 yr old who's parents couldn't visit her everyday, so i spent my days strolling around the floor with her in a hospital carriage... she was HIV positive but showed no signs of damage from the disease... the nurses told me to be careful, so i walked around with a mask on and she was in protective gear... a few nights, she cried, so i would sit with her and stroke her hair until she fell asleep... seeing this poor little girl and knowing that she had a hard life ahead of her, however much time she had... it woke me up to the fact that my life wasn't over...
I don't know if this concept has a name, but I need to call it something. We've all heard about LDL being the bad cholesterol and HDL being the good cholesterol. These lipoproteins are not cholesterol at all but merely carriers. LDL takes cholesterol to cells from the liver and HDL returns cholesterol from cells to the liver. It's a flowing system.
Why does it need a blog entry? Because we haven't got it right. We say simple things like "too much LDL is bad." The problem is, that doesn't cover all the bases, sorry non baseball fans.
What got me thinking about this angle are the fruitarians. Personally I can't stand their cult-like behavior, at least the ones I've read. I'm sure there's a few good apples in the bunch. I have a hard time believing their "interpretation" of science. I see it as "it works for me, so it must be true." We all know that science has to cover all the bases.
But what if the Fruitarians and Atkinsers are both right about heart disease? Can they be? Can we explain it? Obviously if we are both right, it has to be explainable. We just have to figure it out. I think this flow theory might just do that.
So what is this flow theory? I can't give you all the gory details, but guys like Chris Masterjohn can: High Cholesterol and Heart Disease — Myth or Truth? I think what he's saying is that the load of evidence points to oxidyzing LDL as the number one suspect. But things like too much saturated fat, high LDL alone, and physcal experiments do not support the concept that LDL by themselves are in any way dangerous. These are not simple proteins with cholesterol particles stuck to it but complex compounds. One of the things they contain are antioxidants, things that prevent oxydyzation. Further complicating matters are factors such as particle sizes and fat composition -- he says PUFAs are much more prone to oxydization that SFs. His premise is basically this: the longer an LDL is out there floating around, the more it decays. I think we can also add a few others: the less antioxidants packaged in the LDL, the faster it will decay, the more prone the fats contained in it are to oxydization, the faster it will decay, and the smalle they are, the more likely they will get stuck and decay. So lets take a look at these things under three different diets; let's try to measure each diet's atherominity according to this idea of flow or time: the Standard American Diet (SAD), the Atkins (HFLC), and the Fruitarian (F). We'll simply mark them as 0 for good, 1 for indifferent, and 2 for bad. The higher the score, they worse they are.
- - - - - - - - 1 HDL qty - - - - - 2 LDL qty - - - - 3 LDL Size - - - 4 PUFA - - - 5 Anti - - - - - - Total
SAD - - - - - - 2 - - - - - - - - - - - 2 - - - - - - - - - 2 - - - - - - - - - 2 - - - - - - - 2 - - - - - - - - 10
HFLC - - - - - - 0 - - - - - - - - - - - 2 - - - - - - - - - 0 - - - - - - - - - 0 - - - - - - - 1 - - - - - - - - - 3
F - - - - - - - - 2 - - - - - - - - - - - 0 - - - - - - - - - 2 - - - - - - - - - 1 - - - - - - - 0 - - - - - - - - - 5
1. Fructose and excess carb consumption cause high triglycerides which borrow APO B-100s from HDLs thus lowering HDL. Less HDL means LDL stay longer.
2. HFLC will add dietary cholesterol. More LDL means more to clear out so they stay longer.
3. Sugar consumption lowers LDL size. The smaller things are, the stickier they get. The more they stick, the longer they stay stuck.
4. HFLCers eat very little PUFAs while F's avoid SFs but also lower fat intake (affects #2 as well).
5. HFLC lowers need for anti-oxidants (because they work better?) and get many thru high veggie consumption; while F consume more. Add 1 to HFLC if u disagree.
* My weightings are even because I don't kow how to weight them sensically. I debate keeping the size factor.
* This analysis addresses only heart disease forces. I still believe obese people suffer from too much carb consumption for their level of insulin resistance.
It seems according to this flow theory, both low carbers and fruitarians might be right about diet and heart disease. The sure way to fail seems to be SAD. But I'm not a scientist. Don't believe anything I write about this stuff.
As many of you know, I have taken up creative writing as a hobby. I've been drawn to the power of words.
There's a concept writers use to describe effective fiction writing: show, don't tell. There are many examples of this idea. Instead of writing Jill walked down the street, I might write Jill's reflection bounced off store front windows in the early morning light. I'm not saying she's walking, but you might get the sense that she is. I will sometimes try to show instead of tell in my forum posts too, but often it's not that simple. Usually we want to be succinct and get to the point.
This morning I stumbled across a little video which illustrates the power of this concept. Enjoy!