Why is Nutrition Science so Complicated?

Why is Nutrition Science so Complicated?

Consider the following sequence of events:
-In 1945, an 82 day long battle between US Marine and Army forces and the Imperial Japanese
Army was fought in the prefecture of Okinawa. This battle was considered one of the bloodiest
in the pacific and resulted in the death of almost 150,000 Okinawans, roughly a third
of the population. Due to widespread destruction, and foodstuffs
in particular being stolen or deliberately destroyed, a huge number of civilians were
left starving and struggled to return to a sufficient diet after the war. -Just four years later In 1949, data from
US national archives indicated that 85% of Okinawans’ calories came from carbohydrates
with sweet potatoes comprising 69% of all calories and 1% of calories coming from Fish. Then, several decades later, A 2016 paper
pointed out that the Okinawan’s 1949 post war diet has a ratio of protein to carbohydrate
that is similar to an experimental high carb diet used to improve lifespan in rodents. Then just this year In January 2019, a BBC
article referring to this paper comes out with the headline “A high-carb diet may
explain why Okinawans live so long.” Okinawan people did historically eat their
fair share of sweet potatoes – the typhoon resistant tuber made for a good staple crop. However, is it fair to make conclusions about
Okinawans longevity based on their diet right after the war? In any case, when you dig in a bit, it becomes
apparent that this BBC article lacks some very important context. The idea of this video is to give some insight
into the shortcomings of research in order to help you understand what makes for a weak
or strong piece of supporting evidence for this or that health claim. Let’s say a detective wants to determine
who killed John. He will follow clues and investigate evidence
while considering the strengths and shortcomings in each piece of evidence. For example, a witness saying they saw someone
that sort of looked like Count Jackington’s butler is much weaker evidence than a security
camera capturing an image of the butler. It’s good to take a similar approach when
trying to make conclusions from research. Last year, I picked up this book with the
title “The Best Diet: Simple and Evidence based guide to healthy eating” written by
a doctor Tsugawa at UCLA. I saw this book around when I was making a
video on Butter Coffee and the cover of this book has a big red X next to the word “Butter
Coffee” so I picked it up to make sure I wouldn’t have to delete my video. On page 31 that it says “Butter is a bad
fat as shown by several studies.” Now, the first, most obvious step to evaluate
a claim is to investigate the evidence the claim is based on. There’s a reference number next to this
sentence about butter, so I go to reference (4) in the very back of the book and it has
a footnote saying “The idea that butter is bad comes from observational studies in
which butter seems to raise the “bad” LDL cholesterol. However, the evidence that butter intake affects
your risk for disease is not particularly strong.” This footnote goes on to point out that a
2016 paper did not show an association between butter, heart attack and stroke. This book also brings up a very often debated
topic: Eggs. Eggs, especially the yolk, can be a cheap
source of good nutrients like fat soluble vitamins which aren’t contained in the majority
of typically eaten foods. However, the book recommends limiting your
egg intake to only one a day. If only this book came out earlier, then this
poor 88 year old man could have been warned. He ate 20 to 30 eggs a day for 15 years as
of 1991. Interestingly, he maintained normal plasma
cholesterol despite the ludicrous amount of dietary cholesterol he consumed- we’ll talk
about how this affected him in a moment and We’ll come back to why it’s being said to
eat only one egg a day, but before we do that, allow me to explain a couple concepts. The first is that of confounding variables:
Here we have the grabbing headline “High-Fat Diet Linked to Anxiety, Depression.” If we take a look at the study they’re basing
the article on, we see that the high-fat diet they used – D12451 from Research Diets Inc.
, contains 20% protein, 45% fat and 35% carbohydrate – this is relatively high fat. However, half of the carbohydrate is refined
table sugar… by weight there’s almost as much pure sugar as there is fat. So, Do think this might confound the effect
of fat? Now, Biology is incredibly complicated – there
are so many variables that may affect a given output. So, a common challenge is isolating the effect
of one food or gene on disease risk from the effects of all the other foods and genes that
could also potentially increase that disease risk. I had a chat about the various challenges
in scientific research with Eli Lyons,the CEO of the synthetic biology
company Tupac Bio. In his current position, and as a PhD candidate
at the University of Tokyo, Eli has a decade of experience regularly reading through research
papers. Afterwards I followed up on Skype to ask him
about the challenge isolating variables. “In some of my work, I’ve done statistical
analysis on oncogenes or high throughput mutagenesis. Oncogenes are cancer causing genes, or, genes
that when mutated may drive cancer. And, what commonly occurs though is that in
a tumor, for example, you may have many genes that are mutated. However, not all of the mutated genes are
actually driving the cancer. So, the ones that are driving it are called
driver cancer genes. And, so how do you isolate the effects or
determine which genes are the driver cancer genes and which are like carrier mutations. It’s also more complex because there may
be some interactions between the driver cancer genes and some genes that are mutated and
the interactions are very complex, but the impact may be largely due, the majority of
the impact may be due to the driver genes for example. And so, really, it’s isolating how large
of an impact or, how much of the cancer is due to gene A – a mutation in gene A, and
how much of the cancer is due to a mutation in gene B for example.” (2)This brings us to my next point, the importance
of context: A good example for why it’s hard to isolate
things from context is protein. There seems to be some concern about protein
for people on a low carb diet. One of the goals of doing a low carb diet
is keeping your insulin low, and to achieve that people replace the carbs with fat or
protein, but protein ironically seems to raise insulin levels. However, does the context matter? Does protein by itself reliably raise insulin
levels? If we take a look at this study in canines
as presented by Dr. Benjamin Bikman, we see that dogs receiving an infusion of glucose
get spikes in their insulin levels when given the amino acid alanine. So, it looks like protein does raise insulin. But what about dogs without the glucose infusion? The dogs not receiving glucose didn’t see
their insulin change to any noticeable degree. So then, imagine how this fact would confuse
the data in for example a study looking at how protein affects risk for diabetes, an
insulin driven disease. You might look at how many servings of meat
people are having per day and then look at who develops diabetes, but the physiological
effects of a hamburger patty tucked in a whole wheat bun and served with french fries are
going to be much different from a steak served only with butter and rosemary. Another good example of the importance of
context comes from the work of Dave Feldman. Dave is an independent lipid researcher who
has developed something called the Lipid Energy Model. He’s actually been interviewed on this channel
before. We all know that we are supposed to keep our
LDL bad cholesterol as low as possible to prevent heart disease. However, in our interview, Dave explained
the logic behind why when it comes to heart disease, LDL – the so called bad cholesterol
isn’t all that important in the context of high HDL and low triglycerides. That is, you don’t need to worry all that
much about sky high bad cholesterol if your HDL is high and your triglycerides are low. “The NHANES data has certainly been exciting
because while it’s true that if you look at LDL by itself, it’s associated with higher
mortality, when you look at it grouped with high HDL and low triglycerides, it’s associated
with low mortality.” This huge NHANES data set that Dave recently
got his hands on is showing that this idea that HDL and triglycerides are more important
than LDL cholesterol indeed pans out surprisingly well. “I first removed everybody that had a low
LDL, so everyone with 159 mg per dL and lower, I took out. I went ahead and separated out everybody with
HDL cholesterol of 49 or lower. And then finally, I took out everybody above
100mg/dL of triglycerides. This was pretty exciting because now I could
actually look at what the mortality data was that was left. And that mortality was pretty exciting because
not only did they have an all cause mortality that was lower than the average, but, believe
it or not, diseases of the heart were extraordinarily low. The youngest person in that group that was
left over, once all three of these markers were accounted for, was 68. The oldest in the group? 94. And outside of those two, everybody else died
in their 80’s. A total of 18 total deaths from diseases of
the heart, and almost everyone died of old age.” So, let’s go back to that earlier point
about the recommendation to eat only one egg a day. The author of the earlier mentioned book explains
that, according to a 2013 meta analysis, those who ate more than one egg a day had a 42%
higher risk for developing type 2 diabetes than those who hardly ate eggs. What a meta analysis does is pile the data
from multiple studies together to try and make more accurate conclusions. So here’s another point for investigating
a claim – the cumbersome task of actually digging through the referenced study. So, Let’s look at this meta analysis that
reference 3 points to. Then, let’s go to Table 1 and see what studies
are used for the data on Type 2 diabetes. Looking at references 51, 37 and 41 we get
these three studies: The data from this study[37] did suggest that
high levels of egg consumption are associated with increased risk for type 2 diabetes. However, this study[51] found that “No statistically
significant associations between egg consumption and diabetes.” and this other study also
[41] found “no association between egg consumption or dietary cholesterol and increased risk
of incident T2D.” But, by taking these three studies with differing
conclusions and pooling the data together in a meta-analysis, the conclusion becomes
“compared with those who never consume eggs, those who eat 1 egg per day or more are 42%
more likely to develop type 2 diabetes.” At first, this seems like a good idea – more
data, so a more accurate picture, right? However, in this study [37], the women eating
the most eggs are smoking the most, eating higher amounts of trans fat, eating 500 more
calories per day and exercising the least. The men who ate more eggs also drank more
alcohol and smoked more. The researchers do take these unhealthy habits
into account and make adjustments when analyzing the data, but it is very ambitious to assume
you can quantify the effects of all things on diabetes risk, and then subtract these
to accurately understand how just eggs by themselves affect diabetes risk. In any case, the studies used in this meta
analysis not all adjusting for potential confounding variables. This one only adjusts for Age and Sex. This one doesn’t even account for how many
calories the people ate along with the eggs – what if the people eating two eggs a day
are getting those two eggs from a Denny’s Grand Slam seven days a week? By the way, remember the guy who ate 25 eggs
a day for 15 years? The 88 year old had no health complaints other
than poor memory and loneliness after his wife passed away. Also, he had no history of stroke, heart disease
or diabetes. So, while this kind of meta analysis study
is a clue to the puzzle of eggs, I think you’d agree it’s not as strong a piece of evidence
as it appeared at first glance. Of course the other reason for us being told
to not eat eggs comes from the theory that fat and cholesterol cause heart disease. The very first clue for this theory comes
from research by Nikolai Anichkov. Anichkov found that feeding cholesterol to
rabbits had them develop very high levels of blood cholesterol and atherosclerosis. …But rabbits are herbivores, and their natural
intake of cholesterol hovers right around zero milligrams. So, let’s move onto my next point: the shortcomings
of using animals as a model for understanding humans. “We were talking about the problems with
model organisms…” “Yea… The basic idea is that the mice that they
use in experiments are not very diverse. Right, so they’re kind of like clones and…
the way they’re breed is similar to having a breed of dog. If you did all of your experiments on golden
retrievers. Is that really representative of what would
happen if you did the experiment on ten different dog breeds?” To give you a picture of how this can affect
research, consider the work of Lewis Dahl. In 1963, he fed rats a high salt diet and
found that some, but not all developed high blood pressure. He then went on to selectively breed rats,
producing a strain of rats that were genetically sensitive to salt. Then, in 1970, he fed these salt sensitive
rats commercial baby food and about half of these salt sensitive rats died. So he concluded that the high salt content
of the baby food formula was to blame. After his study was published, the US senate
issued a mandate for lowering salt in baby foods. Now, think about that for a moment. Does anything sound odd to you about this
sequence of events? Anyhow, let’s get back to our discussion
on mice models: “…It’s well known that mice models are
not always very good and the pharmaceutical industry knows that really well – it’s really
easy to… there’s a lot of literature on it, but it’s really easy to think about
– which is well, how do drugs get approved for humans? Well, one is they do early stage pre-clinical
work which is usually on cell lines and then on mice and then they move maybe to canines
and apes or something and then they start human trials. But, you may be familiar that with the phenomena
that in clinical trials 1, the drug passed but it failed in clinical 3 trial. But if you imagine like, it failed at one
of these human based trials but, well, it passed the mouse trial. Right, so I think that right there gives you
some idea of that well, the mouse model did not model what we expected to happen in humans. Why does that happen? Well… mouse is different from a human, and
also the model they make where the mouse has a certain type of tumor, that tumor may not
perfectly model the tumor in humans. Diabetes in mouse might not be the same…
like the model they make.” “This situation where like you’ll pass
the mouse phase, but then you fail at the human phase. That’s not a rare occurence?” “Not rare at all, it’s probably the opposite.” With all this said, studies based on mouse
models are still pieces of evidence – not to be completely dismissed whenever we don’t
like their findings. But, we should try and investigate the specifics
of why a particular mouse model wouldn’t be appropriate for emulating humans. “I guess One of the easiest different to
point out is just that their lifetimes are shorter. So… they mature faster. Right, so, I’m just kind of going through
really easy differences to spot between mouse and human … in my old lab I was doing some
retinal development research, like studying how the eye develops, but like, somehow it’s
kind of a weird model to use because mice are born blind… And then like humans are not… so that’s
kind of odd. These are just some things you’d want to
start to think about when you’re thinking is this a good model to use of humans.” Let’s say it’s a typical Saturday morning,
you’ve just made your coffee and are sitting down to read a paper like this one and you
see the words “high fat diet induced obesity.” But you are considering doing a keto diet
to lose some weight, and you think “If a high fat diet is a reliable way to produce
obesity in rodents… Why would I want to do a high fat keto diet?” However, we should first investigate if there
are some specific metabolic differences between rodents and humans. The high-fat diet for the mice used in this
paper, D12492, is 20% protein, 60% fat and 20% carbohydrate. An actual ketogenic diet for humans would
need to be restricted to around 10% or even 5% carbohydrate, but at 20% of calories coming
from carbohydrate, this rodent chow is actually a relatively low carb diet for a human. Now It’s thought that most of the weight
loss magic from a keto or low carb diet comes from lowering insulin and entering ketosis. However, rodents don’t enter ketosis nearly
as easily as humans. According to Dr. Benjamin Bikman, in rodent
experiments, without calorie restriction, to get rodents into ketosis, you need to reduce
their diet down to just 1% carbohydrate, 9% protein and 90% fat. Even a diet that is 95% fat barely rodents
gets rodents into ketosis. By the way, a 95% fat diet would be like an
entire cup of butter and about 80g or 8 thin slices of bacon for the day – but any more
bacon than that would be too much protein. Simply put, the amount of carb restriction
that qualifies as low carb or keto for a human does not qualify for a rodent. These kinda specific differences should be
acknowledged when using rodents as models for humans. Let’s move on to my next point: Food vs.
Compounds in food – We’ll start with chocolate. In his book “Doctoring Data,” Dr. Malcolm
Kendrick talks about a headline he saw saying “Chemicals found within chocolate protect
against heart disease.” He explains that, according to the research,
“catechins and procyanidins, found in dark chocolate, inhibit the enzyme Angiotensin
Converting Enzyme (ACE). When ACE is blocked, blood pressure drops.” This is actually how blood pressure lowering
drugs work, so it makes for compelling reasoning behind a compelling headline. The only catch is that there wasn’t any
actual clinical effect… while dark chocolate did result in an 18% drop in ACE activity…
there was no actual drop in blood pressure in those taking cocoa extract. Another example is the idea that a compound
in such and such food has been found to cause disease, so that food itself must cause disease. For example, there is the idea that heterocyclic
amines in cooked meat cause cancer. However, the studies finding that these heterocyclic
amines are cancerous were giving rodents amounts of HCAs equivalent to 1000 to 100,000 times
the normal amount consumed by humans. As this paper says, “Comparison of the carcinogenic
dose in rodents and the actual human daily intake suggests that the latter is definitely
too low for cancer production to be explicable in terms of HCAs alone.”[R] One last example is red wine – you’ve probably
heard that it protects against heart disease. This review article from the Journal of Cardiovascular
Disease Research discusses the quote “accumulating evidence that suggests that red wine possesses
a diverse range of biological actions and may be beneficial in the prevention of CVD.” However, if we look at the references, most
of them are looking at compounds within red wine – namely polyphenols and resveratrol. One study found that the rat equivalent of
one glass of red wine worth of polyphenols had beneficial effects against heart disease. Then again, does that mean a glass of red
wine itself with its 200mg of polyphenols and 10000mg of alcohol prevents heart disease
in humans? By the way, the other compound in red wine
resveratrol has gained a lot of attention for its promising anti aging effects. However, one of the researchers investigating
this compound has said that, in order to get the anti aging benefits, “the sad news is
you’d need to drink about 1000 bottles a day, which I don’t recommend.” In any case, the point is: claims like “such
and such food prevents or cause disease” are very different from claims like “compounds
in such and such food prevent or cause disease.” My next point on what to consider when evaluating
pieces of evidence, is why and from where certain ideas arose. For example,
why did people think to start looking at red wine to see if it benefitted heart disease? Well, sometime around 1991, people were trying
to make sense of the fact that the French ate very large amounts of saturated fat yet
had low rates of heart disease. One idea was that this so called “French
Paradox” could be explained by France’s high red wine consumption. So This is what’s called an ad-hoc hypothesis
– a hypothesis added to a theory in order to save it from being falsified. In this case, because saturated fat and cholesterol
must cause heart disease, it was assumed that there must be some protective factor in the
French diet. Put another way the logic is “let’s construct
a new hypothesis (red wine prevents heart disease) to explain data that does not support
our initial hypothesis (fat causes heart disease).” Now, just because a hypothesis is ad-hoc,
doesn’t mean it’s wrong, but it deserves scrutiny. And what really deserves scrutiny are things
that go quickly from the idea stage to clinical practice. An example provided in the earlier book “Doctoring
Data,” is how a good idea arguably killed millions of people. From the early 1900’s for about 50 years
or so, it was thought that strict bed rest for about six weeks was the appropriate prescription
for someone who had just had a heart attack. It sort of makes sense, after such a traumatic
event it sounds like it would be best to let the heart rest and keep exertion minimal so
as not to stress the heart. And I really mean minimal – to quote Thomas
Lewis, a prominent physician from the 1930’s: “The patient is to be guarded by day and
night nursing and helped in every way to avoid voluntary movement, or effort.” So what exactly is wrong with bed rest? As Dr. Kendrick explains, First, lying in
bed stationary for six weeks means that there is a very good chance of developing a deep
vein thrombosis (DVT) in the legs. A high percentage of these break off, travel
to the lungs, and block the arteries in the lungs causing a pulmonary embolus (PE) – an
event with a very high mortality rate. In fact, even a several hour plane flight
carries this risk. In 1977, the term “Traveler’s Thrombosis”
was coined for people developing deep vein thrombosis on flights. Low oxygen, low humidity , and low cabin pressure
at high elevations plus sitting motionless in a chair for several hours is a good recipe
for thrombosis. The second issue with bed rest is that without
any exercise, and especially after a heart attack, the heart atrophies very rapidly. It becomes weaker, and deadly heart rhythms
develop, so you are far more likely to die of ventricular fibrillation. Dr. Kendrick estimates that hundreds of thousands
of people were dying from bed rest each year, and this approach wasn’t being questioned
until the mid-1950’s. So where did the idea come from? Well, in 1912 Dr James Herrick of Chicago
published an article titled ‘Clinical features of sudden obstruction of the coronary arteries,’
Where he essentially described the first documented heart attack. In that article, he stated, ‘The importance
of absolute rest in bed for several days is clear’ postinfarction…” To quote Dr. Kendrick “…Herrick managed
to describe the world’s first heart attack in 1912 and then, without missing a beat,
he immediately knew that strict bed rest was an essential form of treatment – for a condition
never before described.” Another example of seemingly good ideas harming
people is that of Hormone Replacement Therapy. It had been recognised that women under 60
had far lower rates of heart disease than men of that age. For various reasons it became accepted that
female sex hormones were what was protective against heart disease. According to Dr. Kendrick, one key piece of
evidence amidst the limited amount of evidence for this concept was a 1987 observational
study – observational studies by the way are widely accepted to be very weak pieces of
evidence in general. Yet, the idea was still accepted so well,
in fact, that replacing the declining female sex hormones in menopausal women became incorporated
into the 1992 American College of Physicians’ guidelines. In the US, failure to prescribe hormone replacement
therapy for menopausal women was akin to medical malpractice. Later, a randomized primary prevention trial
using hormone replacement therapy involving nearly 17,000 women published its results
in JAMA in 2002. This trial found that “…there was a 29%
increase in coronary heart disease risk…” I wonder how many women would have accepted
hormone replacement therapy if they knew the practice originated from a sorta good idea
backed by a weak observational study. My very last point is… the circular situation
where existing ideas can influence research in a way that biases the research towards
acting as evidence for that idea. So… what do I mean by that? Dave Feldman who we spoke with earlier has
a good example of what I’m talking about: “One of my problems with cholesterol research
is it often lumps soft endpoints with hard endpoints and this can be a bit of a challenge
because our existing opinion on cholesterol can make a difference in how the data is recorded. So, to give you an example on the patient
side, let’s say that you and I have a steak dinner tonight and then afterwards we both
go our separate ways. But, each of that night experiences a thirty
minute prolonged chest pain. And for me, this is the warning I had been
hearing about from my doctor this whole time. After all, he’s been telling me about my
high cholesterol and I need to do something about it or I’m going to have a heart attack. Sure enough when I go to the hospital, it
does in fact prove true that I did have a non-fatal myocardial infarction. So all of that data then becomes record. You on the other hand, did also have a myocardial
infarction, but the difference is because your cholesterol has been low, you went ahead
and took a TUMS because you felt like it was heartburn, went to sleep, and that data never
ended up anywhere inside of the hospital record. That’s a big deal is both of us are already
part of a study. But this also plays into the hands of medical
professionals, because after all, if they would likewise have the same opinion that
high LDL is a risk factor just the same as something like C-Reactive Protein, then that
may be relevant for a judgement call on the margins. Certainly a lot of heart attacks that you
survive are not on the margins. And most medical professionals would agree. But, some are on the margins and that’s
a soft endpoint. I like hard endpoints like mortality because
they’re pretty easy to diagnose. Everyone knows whether you lived or died,
and as such, that data is a lot stronger to look at in the long run.” …And, there are several studies that use
the subjective, soft endpoint Dave is talking about here. So for now, this concludes my points on what
to keep in mind when trying determine if a piece of evidence behind this or that health
claim is strong or not. I realize some of this can be confusing or
disheartening and that nobody has time to dig through 50 research papers just to decide
what to eat for breakfast… but for those of you who want to dig deeper things to deeper
understand what makes us healthy and why, hopefully these points serve as tools to help
you analyze articles and research more effectively.

100 thoughts on “Why is Nutrition Science so Complicated?

  1. "Let's say you and I have a steak dinner tonight…"
    "And then afterwards we both go our separate ways."

  2. the guy looks off to the right like his wife is standing there flashing him and he's trying to keep a straight face during the interview

  3. What a confusing video…. one thing I do know is that you're sponsored by the meat and dairy industry, that much is blatantly obvious.

  4. A high carb diet is so counter-intuitive. Throw in some sugar and that's essentially the American diet that is killing us.

  5. Please do a video about BMI measurement system, I weight at 91.8 KG and I have a Muscle mass of 62.2 KG and my hight is 179Cm the, I got a smart scale that told me my ideal weight should be 70KG, now to think about it if I have 62.2KG muscle how is it even possible for all my bones organs and brain to weight just under 8 KGs!! Please do a BMI video!

  6. Never mix fats and carbs together in a meal. Eat protien and fat or carbs and protien. Problems happen when u have fat and carbs together.

  7. Our pre-agriculture ancestors would eat all of the animal, head to tail. I would assume that there is a lot of cholesterol and fat contained within the whole creature. If this diet kept us alive and well, why would eggs be any different than eating organs and muscle meat?

  8. I love red wine but saying red wine gives you a health benefit is like saying
    you get a health benefit from being punched in the head from a boxing glove coated with vitamin E.

  9. Thank you for this informative unbiased video. I would love to see more videos like this. Could you do video about ur weekly diet? It would be interesting to see what do you eat and why. Thanks!

  10. Hey I love your videos. Just going to make a counter-point to the flights DVT risk. I'm in the emergency medicine field. DVT risks do not go up until at least a 12 hour flight and even then only minimally. The medical community is currently decreasing it's risk-assessment for shorter flights.

  11. Sorry this is long BUT I can't not tell my story in the hopes it will help someone and hopefully help others to think logically not emotionally. Epidemiological studies are not accurate!! Just watch a show called secret eaters and you will see that NOONE tells the truth about what they eat. It's all skewed by bias of the individual person. Most people will put down their ideal diet with a splash of their real in there. That's not science!! I feel so betrayed. I was a devout vegan for years and years. All my children were vegan with me. Only one remains vegan for animal reasons, but he is pale, has almost no muscle mass He was a healthy body building teenager before. All of us got really sick after 3 years.
    My son who was born while I was vegan and I running daily before I got pregnant was born mildly mildly autistic and non verbal. Plus I developed a blood clot in my ram towards the end and it became a pulmonary embolism when he was born. WTF!! That was NOT supposed to happen I was a strict whole food vegan. STRICT. NO DAIRY NOTHING. I drank 3 shots of wheatgrass a day. I ate nutritional yeast everyday too. Sprinkled it on everything. MY hair was falling out and my leg hair hadn't grown in years, even pregnant.
    I lost almost ALL of my muscle mass on the vegan diet. Being vegan I have lost 4 molars.
    I know I'm going to get super angry comments but I can't deny what I see with my own eyes and others are seeing it too. I ADORE ALL ANIMALS. BUT we are animals too. My mind has been blown. I watched my mother struggle with being 400 lbs her whole life and dying of brain cancer in her early 60s. She was a microbiologist so I am not ignorant. I am a scientist at heart and the evidence is still comin in. I stopped the fruit and ANY sugars. NO carbs. MY teeth stopped crumbling and my gums stopped bleeding. OMG veganism made me age so quickly too. I didn't have any wrinkles before but now I am scrambling to get rid of them. In 5 years I aged 10. I developed insulin resistance and always had a bloated belly.

    I accidently found Sally K. Norton & Weston Price. I listened and then I looked it up. It all seemed to pan out okay. So, I started keto and eventually easily transitioned myself to zero carb after a year. So then, I took my autistic son off of the vegan diet and put him on the zero carb. He is making leaps and bounds in understand, interaction etc… since a little after the switch. He has even begun to babble. Mind freakin BLOWN. Only been 2 months!!
    On this zero carb my hair and nails have started growing again!!!!! I can't believe it. I have to shave my legs again hahaha. AND it's not so dry and breakable. My muscles started to regrow all by themselves. I am not lifting weights, but I am using a mini trampoline when I watch tv or youtube. Just easy jumping nothing jarring , maybe 10 squats a day. It's all in front of a seasonal light therapy. I cant sit for long at all because the vegan thing crashed my arterial system and I developed varicose veins and massive swelling in my ankles and calves. I also developed a bone spur on the heel off my right foot. Ode to joy 🙂 SO I am not running or anything, I can't. Somebody needs to look into the light therapy thing. It turns my fat soft and squishy when I am in front of it, AND I AM losing my belly, thigh fat, cellulite, fat ass, and bat arms day by day. I can actually see it and feel it physically daily. I am in shock and blown away by all of this. It still blows my mind and goes against EVERYTHING I was ever taught about food and nutrition. MY memory and cognitive understanding has begun to improve. I had a horrible horrible memory for so long, I got tested for Alzheimer's and MS. No lesions. No visible abnormalities or defects in the brain.

    oh..oh.. OXALATES!!!! Oxalates and calcium hhhmmmmm…. When I was in early labor with my oldest son way way back in 97 they gave my a medicine to pull the calcium out of my muscles and omg it was painful. SOooo…. calcium works on muscles in contraction and relaxation right? I went zero carb and the muscle rolls I had in my neck since I was 23 released!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! This is super technical and sciency stuff. The short of it was I stopped the oxalates and my muscles relaxed. I am officially totally RECOVERING FROM FIBROMYALGIA. You will not understand unless you have ever suffered from fibromyalgia, how incredible those words are. Fibromyalgia steals your hope and future. I don't know if it will come back if I reintroduce the oxalates but honestly I lived in pain for so long and we all honestly thought I was dying by 32. My muscles never grew and the constant ache and pain everywhere was stealing my life completely and took no prisoners except me. Now I can fathom a future!! That was not possible before. I am hoping to live to be in my 90s, before it was not even a possibility.

    ALL animals on this planet have a natural diet, and that includes humans. We are animals too. It has been proven time and time again by just about everyone. Ask anyone if you give an animal their natural healthy diet they will be healthy and free of disease. Why on G-d's green earth would everyone think we are any different? Keep It Simple Stupid always seems to end up working the best. Pesticides, fertilizers, gmo plants etc… That's not natural or healthy. We are poisoning ourselves with every bite. Even organic isn't safe because the pesticides and fertilizers are suspicious and not natural. Not all the time but how can you know? A pasture raised animal is not the same as a factory farm animal. Think about what you have to do to an acre of vegetable farming land compared to pasturing an animal. The pesticides, fertilizers, machines, gasoline, tilling, and the acres and acres of land clearing, all those trees and flora. Not to mention how many animals you have now made homeless, not even including the migrating ones!! Then you have to defend your veggies from every animal. SO now you have that procedure to do. Some shoot, trap, or poison. LOOK IT UP. LOGIC. Connect The Dots. If we have to eat them, then it is our responsibility to give them the very best, stress free life possible. Look up the water experiment and emotions and how it affects the water. It's a thinker. If you don't want to keep animals then return to hunting, gathering, but please we must save our home. We share this planet with ALL the animals, bugs, bacteria, viruses, etc.. If you went vegan for the animals you absolutely have to face that fact and reality. Time and time again we find out that human interventions seem to cause more harm then good in the long run. We have antibiotics but at what price? Look up the microbiome and then think about what pesticides are supposed to do to bugs. Our belly bugs have the same pathways!! Think. Connect the Dots. Make FULLY informed decisions, especially when they can negatively affect the world and people around you. Here's another one. I watched a documentary and the guy got hooked up to a machine that would look at his brain when he ate broccoli and then yogurt. The yogurt, his brain lit up and said YES. The broccoli, his brain lit up and said Stop. Now it makes sense to me with the oxalates and lectins. That puzzled me for a long time. The cow's brain doesn't say Stop when it goes to eat grass, it says Yes. The cow's brain says Stop when it eats meat though. The logical conclusion is that our brain knows what's good for us for our millions of years of evolution. We have only been farming for around 10,000 years. We had bigger brains during the freakin ice age. We started farming when it got warmer and our brains have shrunk over 10% since then. OMG That's a HUGE amount!!

    I am sorry for ranting for so long I just can't keep silent anymore. People are dying and lives are being ruined, on both the vegan and the SAD diet. I hope I remembered everything and hit all the important points.

    Listen to your bodies. Be your own best friend. No one can love you quite like you can 🙂 I didn't listen for years to my body and in return she didn't listen to me. I do now and so does she 🙂

  12. I don't fully trust Eli. his eyes say that he's lying but idk if he is just trying to look into different cameras. in the Skype chat he was looking a lot to his right but again I can't be sure because the image could be reversed

  13. I lost about 40 pounds last winter by exercise and calorie restriction. I did not really restrict food type. Just made sure to have a calorie deficit almost every day. About I month after diet ended I settled in about 10 pounds up from my low and am still there. I am currently doing an experiment on myself. I am eating a high carb diet and exercising again. I try to be calorie neutral each day rather than have a deficit. If one of those Keto people looked at what I have been eating in a day they would surely predict some weight gain in my near future. I predict I will not because it is all about the calories! We shall see who is correct.

    I know there is more to nutrition and optimal health than just weight. But when it comes to losing and maintaining weight. I think all these competing diet theories are moot.

  14. Might be interesting if a study was done on difference(s) between eating raw eggs, eggs cooked in low heat and extra virgln olive oil, eggs cooked with corn oil, and eggs cooked with canola oil.

  15. 16:50 but what about studies that don't pass on mouses but would pass in humans and we don't know because we can't just directly make clinical trials on humans firsthand.

  16. clearly we are still in the dark age of health knowledge. Everything is a "MAY" or MAY NOT! i could say that as well. Let s all eat Raw Carrot ffs.

  17. Great topic of discussion! My research also concluded the same outcome and I am still seeking counter evidence to confirm my bias.

  18. Not sure if I've said this before but love watching your video's and I am considering a large donation to ensure you are able to create more videos. We'll have to see come tax time how much I am able to contribute since I'm retired now. I would love to compile my own research and voice it over my own channel but for now I'm just a happy viewer.

  19. Not all eggs are the same. What kind of diet and conditions were the chickens living in? I personally eat organic paster chicken eggs. The taste and consistency is obviously different and I believe that the health benefits out way to cost. Who knows what chicken eggs the old man was eating. I would guess that he was consuming eggs that were not from factory type eggs. To be heather we should get back to nature.

  20. As a physician, I would like to point out that people are mistaken for 1 thing: Physicians are not there to give you diet or exercise recommendations. We have no formal education any any of those except some general principles and the recommendations. That's why I believe that a conjoint work between your physician, dietitian and exercise coach should be your holy trilogy for a good health.

  21. Growing up in NZ from 1957 on we all ate lots of butter and cheese and eggs and meat etc, and desserts and home made baking. But nobody was obese. I rode my bike to and from school and we were required to work hard around the house and garden. My grandmother and great grandmother used to make Scottish oatmeal for breakfast with cream and brown sugar. Home made cookies and cakes and scones with home made jam for morning and afternoon tea. Nobody was obese – and they ate lots of bread too, with meals and between meals. We never heard of eating disorders and allergies and food sensitivities etc……

  22. There´s plenty of people on the internet trying diferents kinds of diets. Hard to believe that you may trust a youtuber more than a nutritionist these days.

  23. I love this channel so much. Most of it can be described as "ways to combat flawed logic" or "how to ask the right questions or find the real issue." Fantastic work!

  24. I've been binging on your health and diet videos over the last week and I have learned so much. Your teaching style is so easy to understand and you always fully explain your points. Thank you SO much for these videos! I honestly believe you're saving lives!

  25. As a broke MSc student I can see things like this: Eggs are a cheap source of protein and vitamins, In case you need cheap food in order to live properly with satiety, it is more likely to endulge into smoking and alcohol consumption. Alcohol and nicotine are the drugs of the poor. If you are poor, there is a high chance that you got chronic stress and anxiety or even depression. That is how eggs are "killing" people.

  26. If the model of using other animals to test drugs destined for human consumption isnt very accurate.. why still use it in the first place? Why cant we just clone vegetable humans and use them for pharmaceutical trials?

  27. if the mouse model doesnt accurately represent the human model and many new drugs fail the final stage of human testing… and the inverse is possible (drugs being fine for humans and dangerous for mice), just imagine how many drugs that may have been seriously beneficial to humanity has fallen by the way side because it as unable to pass animal trials..

    assuming here that drugs are outright rejected at the point of failing mouse trials and no further testing of that drug happens.

Leave a Reply

Your email address will not be published. Required fields are marked *