What I see everyday. Stroke, Dementia, heart disease

(Sophie) #13

What I find interesting is that in the history of the world, people died of infectious diseases, but now, within the last half century, most people are dying of chronic diseases.

(Kee) #14

I am 70 yrs old. I want to get off Prozac which I started taking when my Father became ill in 2014 and died in 2015. I am doing Keto now, have lost 15 lbs in a month which for me is wonderful. Any suggestions?

(Cywgdave) #15

KCKO, if you are feeling better talk with your Dr. about stopping/tapering/reducing the prozac. Can’t remember but if you search on this site for it there is sure to be others with the same/similar questions.

(Cywgdave) #16

Timely post, I just listened to an interview with Gary Fettke on Ketogeek yesterday (I listened yesterday, it was posted about a week ago) He talked about this, the broken system and what’s happening.

To paraphrase (especially as I can’t remember exactly and don’t have the time right now to listen again), he says he and Belinda have decided to stop battling everything and just sit back and watch the train wreck unfold. They will continue to do what they can to help as many people as they can but have realized that trying to fix the system is essentially impossible, it will have to implode and then rebuild itself. He makes some pretty strong statements about Dr’s along the lines of Ken Berry, good Dr’s will go with the evidence and help patients even if it conflicts with guidelines, bad Dr’s will continue to follow the guidelines and as things play out the good Dr’s will eventually be viewed positively.

Not the greatest recollection but that’s the gist of one part of the interview.

Comments on the sickness management system start about 1:05:00 give or take.

Good interview, well worth listening to. Can skip about the first 8-11 minutes of fluff before getting to the Fettke interview.


Yup. My Type 2 Diabetes husband, in end stage renal failure, just had his second heart attack (shortly after his first amputation). In the hospital they put him on a diabetes diet. Then they put him on a kidney diet. Then a low sodium diet. They asked if he was following good diet. I felt like saying “Like what? The one you guys have been advocating? The ones that are killing him?”

(karen) #18

Mmm hmm. I’m visiting with my Mom. She had an issue with gallstones last month, so they took her off her statin (yay, finally), because it was ‘damaging her liver’. :roll_eyes: So her new medical advice is to go absolutely crazy with low cholesterol, low fat and low sodium (but of course keep eating lots of cereals and whole grains) to mitigate the ‘danger’ of removing the statin from her pill parade. So now she’s adding oatmeal and raisin bran to her oj, toast and pastry diet. She’s so confused and tired about all this advice. I feel terrible but I’m not here enough to step in and become a dietician, so her medical team will continue to make her life miserable as they shepherd her toward diabetes.

(Milton Alvis, MD) #19

As as physician for 38 yrs, cardiologist for 30, I have never seen anyone who has not improved their situation by adopting high fat, moderate protein and low carbohydrate.

It is important for people to understand that the medical industry in not about health: http://goo.gl/Blh6rW.

The primary drivers of atherosclerosis, as first published 08/01/1950 http://goo.gl/QMpZiI, have always been the fat carrying proteins, especially the fat delivery LDL-particles: Lower Density (than surrounding water), fat (Lipid in medical jargon) carrying protein particles (which typically transport 3,000-5,000 fat molecules per particle),
Be aware that LDL-C is NOT a measure of LDL particles. its is a number which is not measured from people’s blood sample. It is a guess, Friedewald equation, of how much cholesterol, a fat (made by every cell), is contained within all LDL particles within a 10th of a liter of blood plasma.
This LDL-C value correlates very poorly with actual LDL-particle concentrations, the value which has always most accurately correlated with rates of disease progression and cardiovascular event rates.

The HDL-particles: Higher Density (than surrounding water), fat (Lipid in medical jargon) carrying protein particles (which typically transport no fat, up to a few thousand fat molecules per particle, depending on size) and serve to remove fat molecules (such as in the walls of arteries) from cells overloaded with fats so that they do not die in place (resulting in atherosclerosis).

However, if HDL particles remain small, typical when eating low fat, high carb, HDL particles do not function well. Only the two largest of the 5 groups (by size, density) of HDL particles correlate with lower rates of cardiovascular disease events over time.

Another long promoted lie is that arteries narrow in response to atherosclerosis. Our arteries enlarge: http://goo.gl/xL1roN, http://goo.gl/aRhOU2 http://goo.gl/RgYv8w in compensation which is why, though atherosclerosis, as known from US autopsy studies, from the 1920s on, is typically present in over half the population well before age 10, remains without symptoms for decades until a plaque rupture suddenly shed debris into the blood leading to clots and obstructions downstream (too small to see by any current medical technology, called microvascular disease) and sometime large enough clots to see by angiography.

Because the disease in within the walls of arteries, both angiography &.especially ALL stress tests totally miss the problem until after complications of advanced disease.

Carbs mean sugar and all carbs are only absorbed after digested to no bigger than one or two sugar molecules.

Since, at any given moment, the entire blood stream only contains about a teaspoon of sugar, all excess coming in is rapidly removed by the liver cells, lesser amounts muscle cells, with both have limited capacity for short term storage as glycogen, a carbohydrate.

All excess glucose is converted by the liver into triglyceride fats for storage and shipped out to the body via the fat delivery particles: primarily VLDL & LDL, thus obesity.

After decades of challenges from daily sugar onslaught & rising insulin+amylin outputs to drive sugars into storage, sugar levels rise, eventually enough that the disease industry calls it Diabetes Mellitus, defined as a HbA1c of 6.5% of higher. Yet optimal cardiovascular health corresponds to a HbA1c of 5.0% or lower.

Cholesterol has NEVER been the correct issue, is made by EVERY animal cell https://en.wikipedia.org/wiki/Cholesterol but was promoted by the US government (about 2 decades after politicians sold US citizens on having taxpayers pay for medical services, a power grab for money & power) but then found that the costs (as always) grew far beyond “projections”, typical *.gov politician, bureaucrat & CBO BS.

I hope some of the above details will help some people understand some basics of physiology a bit better.

Milton Alvis


(Bella) #20

What if you are the family member who is looking after themselves?

I have seen men in my family drop dead with heart attacks, my mother with dementia, others with type 2 diabetes and the other health issues associated.

Myself and a brother are the only ones over the years to fight to keep healthy, with exercise and diet. I admit due to 2 years of depression I lapsed - hence why I am on keto now. I NEVER want to go back to how rotten I felt in those bad years.

My worry now is am I going to be the one to look after those that are sick?

Of course I love them with all my heart, but its already stated where either me or my brother are the ones being called out of work to hospital emergencies.
Yes, it could be me that needs care in the future for reasons out of my control. I accept that, and there is nothing special about me.

There is a small resentment building inside me, especially when they don’t want to hear good advice (you just can’t teach people), when I see how badly they eat and drink and their pathetic attempts to tempt me with this crap, the funny thing is their children - my nieces and nephews have healthier attitudes, picked up from school, the net and their friends. I’m one of only a couple of adults able to run around with them at family gatherings.

There is an unspoken bond, so I will be there for the kids as much as I fantasise about packing a bag and taking off far away.

(karen) #21

Nice that your nieces and nephews are picking up on new info. I have a feeling the majority of the boomer generation, even if trying to “eat right”, is going to sicken and die (sloooowly, as they bankrupt medicare), clinging to the sinking ship of cholesterol paranoia, low fat, whole grains and salt deficiency. As with so many other outmoded ideas, these concepts may have to die of attrition. Glad to have set off in a new direction, even if I’m not 20!

(mark) #22

Mark … Age 57, Major subarachnoid haemorrhage stroke on14th of Oct/2014 still standing. MRI shows a second aneurysm. As of yet, no one in the field of neurology has been able to explain to me, without a doubt, the cause. The only residual neural damage is to my motor cortex, left leg. After 3+years I have regained total use of my left-hand side and can walk once more. ( lots of hard repetitious work) Growing up in the 60s,70s and 80s was a different/less hi-tech world. Paleo was a dinosaur and Keto was an Indian that chilled with the Lone Ranger. We were not privy to such advanced knowledge on Holistic ideology and sugar was great stuff.

I don’t want to waffle on about it but please try not to be too harsh.

I’m trying to get my ears around Ketosis and how it affects the internal digestive system. How the different fats impact the brain, the changes to insulin functions and the hormonal impact on Thyroid processes.
I’m a tradesman not an academic so if anyone has any good reading suggestions it would be very much appreciated. I also think that the Standard Australian Diet would be somewhat similar to yours.

(Andrea) #23

I had my SAH at 39, 3 years ago. I was very fortunate that other than tiredness I’ve no deficiencies. One aneurysm coiled and another being monitored. I’ve got my yearly scan next month and at that stage I’ll have been on keto 1 year. I’m intrigued to see if anything will have changed (the coiled one is only partially occluded).

I’m with you trying to understand the “why” but I’ve no answers…no risk factors, no smoking, no family history etc. So much so I was initially sent home as “yeah it’s just a migraine!” My only thought is that at the time I’d been on a relatively low-fat, low-protein diet. Plus I’m sure excessive exercising was the final straw that made my poor wee aneurysm to burst!

The one thing that frustrates me looking back is the diet that was available in hospital. At the time my diet was no grains, no nuts, no nightshades, limited diary, no meat, only fish for protein (yeah I was’t eating much!!!). In the end I got my hubby to bring in “fresh and healthy” food every day. Still, if I’d been on keto then I’d have just been getting him to bring the HWC and cheese! :slight_smile:

(karen) #24

I’m not sure if you were responding to me or just harshness in the thread in general. I’m not trying to be harsh on patients / consumers - and I’m a boomer myself. I just think these poor ideologies are entrenched in our medical establishment and to some extent, in our own brains. I’m watching my mom enthusiastically embracing the science of 1985 that her doctors are (apparently) still feeding her.

This is one good reading list, Kevin B made an awesome ‘book report’.

(mark) #25

No not anyone specifically just the lack of tolerance in general, if your not happy in your chosen profession move on or take some time out for yourself. ( The original thread ) My second embolism has been left for my body to reabsorb, so naturally, I’m trying to find the most efficient/healthy diet to meet my needs. If nothing else this has been an enormous learning curve. And thank you for the reading suggestions.
After all, life is short so it should be sweet.

(karen) #26

No no no, life is short BECAUSE it’s sweet! Life should be long and salty, like bacon. :stuck_out_tongue_winking_eye: :hugs:

(Ken) #27

OK Doc, I’ve a question for you. Since HDL, if I read it right, has the ability to reduce amyloid plaque and threrfore alleviate Athero, what role does circulating ketone bodies play? I have always considered it probable that they also play a role in plaque reduction as they are essentially solvents, so their effect would be similar to the effects of alcohol on chronic alcoholics, preventing the accumulation, of plaque.

(Milton Alvis, MD) #28

Amyloid refers to proteins: https://www.google.com/search?q=Amyloid, Not atherosclerosis.

Plaque is a catch-all term for accumulations of materials within tissues in many different diseases, including around teeth, under gum line. It is not at all specific for atherosclerosis.

Atherosclerosis is an accumulation of living and dead white blood cells within the walls of arteries. The cells are ingesting fat carrying lipoprotein particles which have become oxidized. The overlying endothelial cells express surface proteins triggering monocytes to stop, squeeze out between gaps between the endothelial cells into the space below the endothelial cells, transform into macrophages and ingest the oxidized lipoproteins.

If the macrophages stay too long, ingesting more and more lipoproteins, become foam cells (refers to their appearance under a high resolution microscope, oil-immersion lens) and subsequently die in place releasing all their fat membranes and ingested fats, then the atherosclerotic process starts and can proceed.

Typically starting in childhood, the disease become more and more complex over decades, though the muscular wall of the artery stretches out to make room for the accumulations, thus zero lumen narrowing or symptoms for decades until plaque ruptures, debris and clots block blood flow; most events without symptoms which people or physicians ever recognize.

The old term “fatty streaks” was started by a pathologist who thought the early deposits (autopsies of children who died for other reasons) looked (grossly) like fat deposits under the endothelium lining of arteries (even though no adipose cells are present) over atherosclerotic deposits.

Lipoproteins are complex assemblies of proteins (made & excreted into extracellular water by liver and intestinal cells) which transport all fats (lipids in medical jargon). They have long been divided into 5 major groups by density compared to the surrounding water and are the primary driver over atherosclerosis, as first published 1950: http://goo.gl/QMpZiI.

The separation method was density compared with the surrounding water. Thus: Higher Density than Water Fat Carrying Proteins (HDL), Lower Density than Water Fat Carrying Proteins (LDL), Intermediate Density compared with Water Fat Carrying Proteins (IDL), Very Low Density compared with Water Fat Carrying Proteins (VLDL) & Ultra Low Density compared with Water Fat Carrying Proteins (ULDL). The last group historically called Chylomicrons, and the only ones, if very large (~1,000 microns), can be seen under a light microscope.

A single LDL particle typically transports ~3,000-6,000 fat molecules.

Which fat molecules? Whichever ones are present. Cholesterol (made by every animal cell on the planet: https://en.wikipedia.org/wiki/Cholesterol) is only one of the fat molecules being carried.

For comparison, red blood cells are typically ~7,000 to 8,000 microns outside diameter yet routine pass through ~5,000 micro capillaries because of their biconvex shape & ~30% cholesterol molecules within RBC membranes which enables flexibility (researchers use the term “fluidity”).

LDL through ULDL fat carrying proteins are fat delivery particles to cells throughout out entire body. HDL particles are fat remover particles.

HDL particles have also long been divided into 5 subgroups. By what characteristic? You guessed it: density compared with surrounding water.

If HDL particles remain small flat disks with a single Apo-A organizing protein, like out body makes them, are they carrying any fat? No, fat molecules take up space and enlarge the particles if being carried.

So which of the 5 sub-groups of HDL particles correspond to lower rates of cardiovascular events? Only the two largest. Liposcience terms these two groups Large-HDL (very practical).

ZERO evidence (or reason to believe) that ketone bodies, a complex group of molecules (from liver gluconeogenesis converting fats into glucose), have any value for atherosclerosis regression.

Physiological processes, though compliant with all known chemistry principles, are vastly more complex than just simple inorganic chemistry.

HDL particles are fantastically complex, 1, 2 or 3 Apo-A proteins per particle (depending on size) along with 80 to 100 helper proteins (still poorly understood) and many issues, including how they function, share fat molecules back to LDL particles (a CETP function) remain poorly understood.

The most potent Apo-A for atherosclerotic regression is Apo-A-Milano, a rare mutant form of the Apo-A protein, first discovered in a few residents of the small isolated town Limone sul Garda in northern Italy in the early 1980s.

After about two decades of expensive research by Esperion pharmaceuticals and impressive results to reverse atherosclerosis (in only 5 weeks in a small trial of administering two different doses of Apo-A-Milano, produced in E. coli bacteria, compared with placebo: https://jamanetwork.com/journals/jama/fullarticle/197579), the over four decades of work on Apo-A-Milano and hundreds of millions spent in research, still no commercially available variant exists which works.

Jim Otvos’ methodology and his company: LipoScience (which developed the Vantera analyzer, https://www.youtube.com/watch?v=OkKn4pLY3AU, over two decades of expensive entrepreneurial research work) remains the ONLY available both validated & reasonable cost technology to measure both lipoprotein particles and particle size.

Yet there remains a huge number of poorly understood issues & commonly promoted yet untrue ideas, including among researchers.

The medical industry has long promoted simple attractive-sounding ideas which turn out, over time (with very slowly advancing knowledge) to be bogus, not infrequently harmful.

Living creatures are high-tech, medical industry low-tech and science is only a method, extremely difficult to perform well, routinely promoting ideas which turn out to be not true. Study: http://goo.gl/Blh6rW

Another basic issue: Living creatures reflect extremely complex engineering. Yet do most physicians have much, or even any, engineering experience? No!

The video “Science For Smart People” is a reasonable introduction: https://www.youtube.com/watch?v=y1RXvBveht0

What group of people started promoting cholesterol even though they knew, from over 20 years of research, that it was not the correct issue?
The government (nearly 2 decades after starting Medicare), specifically the NIH.
Money. (In the 1970s: Several hundred for cholesterol, ~$5,000 for lipoproteins.)
Less expensive to measure.
But does cholesterol correlate well with LDL particles?
No! Commonly quite discordant.

What is the average cholesterol, in the US (from over 2 decades of retrospective data), prior to people having obvious heart attacks (ST-elevation myocardial infarctions, in medical lingo). Answer: 170 mg/dL, which the government continues to term “normal”.

Medicare has fully paid for NMR lipoproteins since available in the later 1990s.
What does LipoScience (Now owned by LabCorp) charge for NMR lipoproteins? ~$80.
Is it available for a lower copay when commercial insurance will not pay?
Yes. ~$14 when sent via Cleveland (thought the Cleveland Heart report presentation is very misleading compared with the LipoScience presentation.)

Milton Alvis

(Edith) #29

Thanks for taking the time to write such detailed explanations.

(Chrissy Calabrese) #30

Great rant! That’s it! I was telling my best friend that I was blessed to have a father who was reading the nutritional literature and cutting edge nutrition in the 1960’s. He applied it to our eating at home and I saw him, juice, drink flax seeds, eat all kinds of interesting things and take lots of supplements but most of all he cultivated a culture of concern. His 4 children grew up with this and we all work at it. There are some things, we can’t control but we can certainly lower our exposure and give ourselves a fighting chance.

Thanks for the rant and keep it up!

(Bunny) #31

Even if the Ketogenic Diet is not something one would want to follow or adhere to, too much sugar is the number one concern whether it comes from carbs, processed carbs or sugar itself.

Simply staying away from processed foods and why eating too much sugar and carbohydrates is bad for us is a start without the “keto” connotation when we play with the “Ketogenic Diet-LCHF” terminology that is like asking asking for a war, you may win the battle but you won’t win the perpetual war with fascist corporate control of governments, if your not eating the sugar and processed carbs, they make no money and pharmaceutical companies go bankrupt, including the banks themselves (Ludwig).

Every time we slam down massive amounts of sugar and processed carbohydrates like there is no tomorrow, the set point (Fung) damage begins, like winding a spool of thread that takes an equal amount of time (months-to-years) to unwind, the type of foods we eat today are not something we would conveniently have acccess to, if there were no processed foods to eat let’s say 1,000 years ago…

Most of the health problems that lead to mortality could be reduced and possibly snapped out of existence if some very sane and basic principles (lowering sugar intake with a little more fat) could be implemented with-out the emphasis being placed on a hardcore Ketogenic regimen?

Eating Whole Organic Natural Foods (metaphor; straight from the vines of Eden or hunt and gather?)


Processed foods;

Processed oils/fats (oxidized/rancid)

Grains (not used within 48 hours of being milled)

Refined Starches

Refined Sugars

Meat if processed even with LCHF?

High fiber all-bran cereal with zero net carbs - Keto friendly?
(Milton Alvis, MD) #32

You are welcome, a complex topic.

Because of your thank you, I added some additional highly relevant detail.