Why Lowering Your Blood Glucose With Medications Is Killing You


Hello and welcome back to Be A Loser. Previously we discussed why there is no cure
for Type 2 Diabetes. If you remember, this is a disease that has
been recorded for many hundreds of years and was actually quite well controlled even a
hundred years ago. But we now find ourselves in an epidemic of
T2D that appears to be a freight train out of control and barreling ahead into oblivion. We discussed how greed is what is truly driving
that train, but even if the powers that be don’t want a cure for the disease, shouldn’t
we at least be able to control it better than we are with modern medicine and technology? Well the problem with that lies in the flawed
concept of how and what to treat with T2D. In order to answer that question we must understand
the mechanism of obesity, the markers of type 2 diabetes, and how lowering blood sugar is
actually making people more sick. So as we know, obesity is very often the herald
of impending T2D. Not always as we saw in a previous video,
but often. So the natural conclusion is that obesity
is a main cause in metabolic syndrome and a marker
of disease. Metabolic Syndrome, as you may recall, is a clustering of at least three of the following medical conditions: Abdominal obesity, high blood pressure, high blood sugar, high serum triglycerides, and low levels of high density lipoproteins, HDL. But in reality obesity is the body attempting
to protect itself from the disease itself. I know, I know, how can getting incredibly
fat be protecting me against anything when I’m told by every doctor, friend and family
member I know that I’m going to die of a heart attack if I don’t lose weight. Well let’s look more closely at the process
of becoming obese shall we. There is a rare disorder known as lipodystrophy
in which the body cannot produce fat. There was one very famous case of this just
a few years ago that was covered by New York Times journalist Gina Kolata. In this article Gina describes the case of
Claire Johnson who suffers from lipodystrophy. Claire was always hungry and very, very skinny
because she did not have fat cells. Even though she was so skinny, Claire found
out that she had a huge fatty liver, polycystic ovaries and incredibly high triglyceride levels. These should sound familiar to anyone diagnosed
as obese as they are all markers of obesity. Claire was diagnosed with lipodystrophy by
Dr. Simeon Taylor who had several other patients suffering from the same disorder. These patients had the worst insulin resistance
he had ever seen, but not one single subcutaneous fat cell that he could detect. These patients typically developed high blood
pressure and T2D which as we know are associated with obesity. So once again one would think, well there
you go, the obesity is causing all these problems. Aha, not so fast. In studies of rats with lipodystrophy, when
the rats had some fat cells transplanted into their bodies. Lo and behold their metabolic syndrome disappeared! The fat was actually protecting the body from
Insulin Resistance rather than causing it. So if the obesity isn’t the cause of the
disease then what is. Well we know that it’s the hyperinsulinemia
or high blood insulin. To understand the nuances and mechanisms of
insulin resistance please refer to my video on it. What’s important for this video is that
when the liver has too much glucose and fat it tries its hardest to move that fat out
as triglycerides. Normally this is done by sending the TG to
the fat cells. These cells, known as adipocytes, are specifically
designed to store this fat. Having more of these cells is not particularly
bad. Other than taking up a lot of space all they
really do is hold fat. That’s their purpose. They have another purpose as well. When these fat cells expand, they release
leptin. Leptin is a satiety hormone and signals us
to stop eating. Unfortunately when we’re obese we’re constantly
stimulating leptin release and as we know from my IR video, constant stimulus leads
to resistance. So over time we become leptin resistant and
our hunger returns. Now being obese isn’t really a problem as
long as all the fat is in the adipocytes. The real problem occurs when you get fat where
it isn’t supposed to be. Fat in the organs. Visceral fat. First it gets stored up in the liver. Fat is not suppose to be in your liver. The fat cells want to store the fat. It’s safe in there. It’s not safe to have fat in your liver. So the liver tries and tries to get it out,
but because of the hyperinsulinemia, insulin is forcing all that fat and sugar back in. Now in Claire Johnson, or someone with lipodystrophy,
there are no fat cells to store the excess fat and so it has nowhere to go but the liver. So to protect itself from this toxic fat and
sugar the liver becomes insulin resistant. So the resistant liver starts spewing out
all this excess triglyceride and our blood TG levels go up. Classic metabolic syndrome. And as more and more of this excess fat is
released by the liver it has to go somewhere, It’s moved around in the body to accumulate in other tissues. so that’s how we get fatty muscles and eventually
a fatty pancreas. As we’ve seen in another video, as the pancreas
gets fat it starts to produce less insulin and potentially even halt the production altogether. The pancreas is designed to protect us. If we have too much insulin then there is
no sense in creating more. So this hepatic IR and impaired beta cell
pancreatic function results in increased blood glucose, but this is a response to too much
insulin. The kidneys normally reabsorb all the glucose
that passes through them. But when glucose levels rise too high the
kidneys cannot reabsorb it all. The natural response when this blood glucose
gets too high is to urinate it out along with loads of excess water resulting in weight
loss. This is the body’s way of lowering the blood
glucose in order to reduce the blood insulin. All of these factors: obesity, IR, elevated
TG and beta cell dysfunction are the body’s protective mechanism against the same thing:
Hyperinsulinemia But when we seek the help of a healthcare
professional, they focus solely on the hyperglycemia. It’s that symptom of T2D that is treated
instead of the true cause. Now before we move forward let’s look at
what can be expected from a lifetime with T2D. As we know, we have many, many drugs that
can very tightly control blood glucose. But even with this degree of control we end
up with damage to virtually every system in the body. This damage is known as End Organ Damage. There are two types of complication: microvascular,
meaning small blood vessels; and macrovascular, meaning large blood vessels. Most organs such as the eyes, liver, kidneys
and nerves are filled with small blood vessels, so damage to these vessels causes the organs
to fail. As we know, damage to large vessels creates
plaques which then rupture and cause blood clots leading to heart attack and stroke. There is a third category of T2D damage that
it’s difficult to classify. So let’s run through the list of diseases
associated with T2D. Retinopathy T2D is the leading cause of new blindness
in the US since 2011. Retinal damage is one of the most frequent
complications of T2D. The damage to the vessels in the back of the
eye causes blood and other fluids to leak into the eye. Over time this can lead to scar tissue which
then lifts and detaches the retina. This can lead to blindness. Nephropathy Diabetic kidney disease is the leading cause
of renal failure. This is defined as kidney failure needing
dialysis or transplant and accounted for 44% of new cases in the US in 2005. It’s estimated that the cost to the US for
the care of this disease is roughly $32 billion. Neuropathy Diabetic nerve damage affects about 60-70%
of all T2D patients. There are many kinds of nerve damage, but
the most common is damage to peripheral nerves. This would include the hands, feet, arms and
legs. The symptoms which are worse at night include:
tingling, burning, pain or numbness. Over time there is a loss of sensation which
leads to joint damage and carpal tunnel syndrome. In some cases it is the autonomic nerves that
are affected. These nerves control involuntary functions
like breathing and heartbeat. If they’re severely damaged it can lead
to sudden and unexpected heart attacks. Ultimately there is no real treatment for
this damage, it can only be prevented. Atherosclerosis This artery hardening and plaque build up
leads to heart attack and stroke. T2D greatly increases this risk. The amount of death and disability from this
macrovascular disease is far beyond that of the microvascular diseases. Heart Disease This is the most feared and recognized of
all T2D complications. According to the American Heart Association,
at least 68% of all type 2 diabetics over age 65 will die of heart disease. This percentage is so high that controlling
CVD is the number one goal for diabetic patients. Evenso, a T2D patient is at three times more
risk of heart attack than a non-diabetic. Stroke This is the third leading cause of death in
the US and the leading cause of disability. T2D increases the risk factor for stroke by
as much as 150-400%, rising 3% for each year with T2D. It’s estimated that about 25% of all new
strokes occur in T2D patients and 16% of all type 2 diabetics over age 65 will die from
stroke. Cancer Many common cancers are related to T2D and
obesity. Breast, stomach, colorectal and kidney are
just a few. The survival rate of these for T2D patients
is often far lower than non-diabetics. Peripheral Vascular Disease PVD is caused by the blockage of blood vessels
going to the lower extremities. The progressive narrowing of the blood vessels
starves the legs of oxygen. Diabetes, along with smoking, is the strongest
risk factor for PVD. Pain or cramping when walking is the most
common symptom. Approximately 27% of patients will have progressive
disease which significantly reduces mobility leading to long-term disability. Some PVD patients may suffer from the next
organ damage. Diabetic foot ulcers Most foot infections are quite rare, except
in T2D patients. This often leads to hospitalization and amputation. Even with tight glucose control, 15% of all
T2D patients will develop a non-healing foot wound. This accounts for over 50% of all amputations
in the US. Fatty liver NAFLD or non-alcoholic fatty liver disease
is caused by storage of triglycerides in the liver exceeding 5% of the livers total weight. This is the leading cause of cirrhosis of
the liver in North America. It’s estimated that about 75% of T2D patients
will develop this. Alzheimer’s disease As we know this is a neurodegenerative brain
disorder causing memory loss. It’s also the most common form of dementia. The link between it and T2D grows stronger
and stronger to the point of many wanting to classify Alzheimer’s as Type 3 diabetes
due to the primary role of insulin resistance in the brain. So why am I pointing all of these horrific
consequences out to you? Well it’s not meant to scare you. I mean most diseases affect one organ system
of the body. But somehow T2D affects multiple systems all
across the body. I mean it’s the leading cause of:
Blindness, kidney failure, CVD, stroke, amputations, dementia, infertility, nerve damage. This disease has been around for centuries
and yet this end organ damage is getting worse and worse? WHY?? Because our current treatment is flawed. The UKPDS, United Kingdom Prospective Diabetes
Study, was undertaken to see if intensive blood glucose control would prevent all this
excessive organ damage. One group of patients was given tight blood
glucose control using sulfonylureas and insulin while the other group made dietary changes. It was believed that high blood sugar was
the cause of all this damage and that this tight control group would fare better. The drugs significantly lowered the blood
sugars. Over 10 years the average HbA1C in the control
group was 7% versus 7.9% in the diet group. However, weight gain was far worse for this
group, and especially for the insulin group. They averaged weight gain of 8.8 lbs or 4
kgs. This was surprising to the physicians at the
time. They could find no benefit for CVD despite
reduced blood sugars. In a sub-study the researchers looked at metformin. Once again there were two groups. One on metformin and the other with dietary
changes only. Over 10 years the HbA1C of the metformin group
averaged 7.4% versus 8% of the diet group. However, unlike the previous study there was
a 36% DECREASE in death rates and a 39% decrease in risk of CVD. So metformin fared better than SU and insulin
even though it didn’t control blood sugars as well. So this implies that while glucotoxicity is
a factor, it’s clearly not the only factor. If we look closer at these results what can
we ascertain? What’s the difference between an insulin/SU
group and a metformin group? And the answer is increased insulin levels. Both sulfonylureas and insulin increase insulin
levels overall. Metformin does not. The problem is that after a 10 year follow
up the SU/insulin group did see a 13% reduction in death rates. While this isn’t as good as the metformin
group, it was good enough for researchers to recommend treating glucotoxicity for T2D. In 2008 the Action to Control Cardiac Risk
in Diabetes or ACCORD study was undertaken to once and for all show everyone, everywhere
that controlling blood glucose was the answer. Other studies had shown that there’s a link
between lower blood sugar and better health and this of course aligned with the prevailing
theory that glucotoxicity is the main concern of T2D. While this worked for type 1 diabetics the
UKPDS couldn’t show that it was effective for T2D. The ACCORD study hoped to show just that. There were two groups: a standard therapy
with an A1C of 7.5% and an intensive group with an A1C of 6.5%
So we got the blood sugar nice and low in that group, but now we have to see some health
benefits. And sadly the intensive therapy group had
an increased death rate of 21% This group was following the advice that was
given to type 2 diabetics by every doctor, everywhere in the world. Lower your blood glucose as much as possible. And yet they were dying at a significantly
faster rate than those with loose glucose control. Due to this the ACCORD study was forced to
conclude 17 months early. It was clear that lower blood glucose with
medications was not effective and even dangerous. But here we are still prescribing insulin
and blood glucose lowering medications to type 2 diabetics when no fewer than 6 randomized
trials have confirmed that these treatments are largely useless for T2D patients. Are we really that clueless? We know from Claire Johnson that the real
problem is high blood insulin levels as well as high blood sugar. So we must treat the high insulin. Raising insulin in an effort to lower blood
sugar is not helpful and ultimately destructive. As organ failures and vascular complications
get worse we must accept that the current treatment for T2D is flawed. Focusing only on glucotoxicity from hyperglycemia
as the only cause of T2D leads us to our flawed and dangerous treatments. These treatments undermine the protective
factors we discussed in regards to obesity and keeps the excess glucose from being urinated
out continuing the downward spiral of the body that ends with organ damage and death. So what would happen if instead of blocking
this protective mechanism you actually enhanced it? Well that’s the purpose of a class of drug
known as the SGLT-2 inhibitor. This type of drug lowers the renal threshold
of glucose so that you do urinate out the glucose. Incidentally this is exactly what happens
in uncontrolled T2D. The EMPA-REG study released in 2015 used one
of these drugs and reduced risk of death by 38% and risk of CVD related death by 32%
Wow it’s amazing what we accomplish when we actually lower the blood insulin and blood
glucose. If we didn’t treat the T2D at all we would
most likely have achieved the same results. Metabolic syndrome is marked by two main issues:
glucotoxicity and insulin toxicity. We achieve nothing by increasing insulin toxicity
to lower glucotoxicity. This is what occurs when doctors prescribe
sulfonylureas or insulin. Of course it makes much more sense to treat
both markers of the disease. This is what the SGLT-2 inhibitor drugs do,
but diet can do this as effectively. LCHF and Intermittent fasting. Ultimately all of the aspects of metabolic
syndrome including obesity and T2D are caused by the same thing. It’s not insulin resistance, it’s insulin
itself. Hyperinsulinemia. But doctors and specialists are slow to understand
this and remain focused on the hyperglycemia and glucotoxicity. And of course as we know, pharmaceutical companies
are all too happy to help keep the focus here as well since it makes them lots and lots
of money. So to sum up here, taking drugs to lower blood
glucose by increasing blood insulin will ultimately worsen your T2D and most likely result in
debilitation or death. You can fare well using a different class
of drug that does not increase insulin levels, but why take a drug at all when you can affect
the same changes through simple dietary intervention. Doctors are not trained in nutrition. Their job is to give you a drug to control your disease. And they’re trained to focus on the high blood sugar, and to treat that with drugs. This perpetuated by the pharmaceutical companies that manufacture and profit from these blood sugar lowering drugs. Drugs have many numerous and serious side
effects. Eating a low carb, high fat diet and even
more powerful intermittent fasting is simple to do, highly effective and lacks any serious
side effects. If the result is that there is even a chance
of reversing your T2D as well as eliminating the potential of all end organ damage discussed
previously, then the answer to me seems very obvious. But of course you must ultimately decide for
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treating T2D that actually benefits those affected by it rather than those profiting
from it. As always from the bottom of my heart thanks
so much for watching, And until next time
Keep Being A Loser!