Where you can find more information

Summary: Extensive research has demonstrated the efficacy of the LCD to improve the most robust CVD risk factors, such as hyperglycemia, hypertension, and atherogenic dyslipidemia. Our review of the literature indicates that statin therapy for both primary and secondary prevention of CVD is not warranted for individuals on an LCD with elevated LDL-C who have achieved a low triglyceride/HDL ratio.

https://pubmed.ncbi.nlm.nih.gov/35938780/

Dietary sugar is not required to keep your organs running correctly. The body can create GLUCOSE in the liver with a process called Gluconeogenesis.

Summary: evidence-based dietary recommendations for FH

Dietary recommendations for CHD prevention in FH individuals for the past eight decades have focused on targeting serum cholesterol reduction with a low saturated fat, low cholesterol diet. However, these recommendations are based largely on the antiquated and evidence-free diet-heart hypothesis. We have proposed that a revision of dietary recommendations for FH is justified, based on substantial evidence that the subset of FH individuals that develops CHD exhibits risk factors, such as enhanced thrombotic risk and a heightened sensitivity to risk factors associated with an insulin-resistant phenotype (elevated TGs, blood glucose, HbA1C, abdominal obesity, hyperinsulinaemia, hsCRP, low HDL, hypertension).

Our assessment of the literature is consistent with the conclusions of Gjuladin-Hellon et al,55 in their systematic review and meta-analysis on LCD and CHD risk: ‘Large RCTs of at least 6 months duration with carbohydrate restriction appear superior in improving lipid markers when compared with LFDs. … Dietary guidelines should consider carbohydrate restriction as an alternative dietary strategy for the prevention/management of dyslipidaemia for populations with cardiometabolic risk.’ Therefore, the evidence basis is sufficiently strong to provide the rationale for clinical trials to be conducted to determine if an LCD would prove to be effective in reducing the incidence of coronary events in FH individuals with an insulin-resistant phenotype or increased thrombotic risk.

https://ebm.bmj.com/content/26/6/295

Summary: The present review integrates a historical perspective on the LCD with a critical assessment of the persistent concerns that consumption of saturated fat, in the context of an LCD, will increase risk for CVD.

https://pubmed.ncbi.nlm.nih.gov/32773573/

Conclusions

A wide range of different studies have shown that high LDL-C is not the main cause of premature CVD among people with FH nor in the general population. There is much evidence that it is only a few people with FH who die prematurely and that the cause in most cases is due to various coagulopathies which they have inherited as well.

https://www.mdpi.com/1422-0067/23/16/9146

Conclusions

This MR study demonstrated no significant causal relationships between red/processed meat intake and the risk of the four CVD outcomes examined. Further investigation is warranted to confirm these findings.

https://www.sciencedirect.com/science/article/pii/S240545772400038X

Summary:

Contrary to previous advice, five new systematic reviews suggest that most people can continue to eat red and processed meat as they do now. The major studies have found cutting back has little impact on health.

https://www.sciencedaily.com/releases/2019/09/190930215122.htm

Results: Worldwide, bivariate correlation analyses revealed that meat intake is positively correlated with life expectancies. This relationship remained significant when influences of caloric intake, urbanization, obesity, education and carbohydrate crops were statistically controlled. Stepwise linear regression selected meat intake, not carbohydrate crops, as one of the significant predictors of life expectancy. In contrast, carbohydrate crops showed weak and negative correlation with life expectancy.

https://pubmed.ncbi.nlm.nih.gov/35228814/

By: Jama Network

Results: During 18 years of follow-up, there were 801 incident cases of diverticulitis and 383 incident cases of diverticular bleeding. We found inverse associations between nut and popcorn consumption and the risk of diverticulitis. The multivariate hazard ratios for men with the highest intake of each food (at least twice per week) compared with men with the lowest intake (less than once per month) were 0.80 (95% confidence interval, 0.63-1.01; P for trend = .04) for nuts and 0.72 (95% confidence interval, 0.56-0.92; P for trend = .007) for popcorn. No associations were seen between corn consumption and diverticulitis or between nut, corn, or popcorn consumption and diverticular bleeding or uncomplicated diverticulosis.

https://jamanetwork.com/journals/jama/fullarticle/1028647

Abstract

There are many strongly held beliefs about constipation that are not evidence based. The purpose of this review is to address these beliefs concerning various aspects of constipation. There is no evidence to support the theory that diseases may arise via "autointoxication," whereby poisonous substances from stools within the colon are absorbed. Dolichocolon, defined as an elongated colon, should not be seen as a cause of constipation .....

https://pubmed.ncbi.nlm.nih.gov/15654804/

Background

The consumption of dietary protein is important for resistance-trained individuals. It has been posited that intakes of 1.4 to 2.0 g/kg/day are needed for physically active individuals. Thus, the purpose of this investigation was to determine the effects of a very high protein diet (4.4 g/kg/d) on body composition in resistance-trained men and women.

https://bit.ly/3Jdj7Tm

Overview

Neural systems that evolved to motivate and reinforce foraging and food intake also underlie drug seeking and self-administration. The fact that some of these drugs can cause addiction raises the logical possibility that some foods might also cause addiction. Many people claim that they feel compelled to eat sweet foods, similar in some ways to how an alcoholic might feel compelled to drink. Therefore, we developed an animal model to investigate why some people have difficulty moderating their

https://bit.ly/43Qqzxg

Abstract

Objective To determine the effects of diets varying in carbohydrate to fat ratio on total energy expenditure.

Design Randomized trial.

Setting Multicenter collaboration at US two sites, August 2014 to May 2017.

Participants 164 adults aged 18-65 years with a body mass index of 25 or more.

https://www.bmj.com/content/363/bmj.k4583

Background

High protein diet has been known to cause metabolic acidosis, which is manifested by increased urinary excretion of nitrogen and calcium. Bodybuilders habitually consumed excessive dietary protein over the amounts recommended for them to promote muscle mass accretion. This study investigated the metabolic response to high protein consumption in the elite bodybuilders.

https://www.tandfonline.com/doi/full/10.1186/1550-2783-8-10

Abstract

This review addresses the role of fat in beef palatability and healthfulness. Particular emphasis is placed on the content of oleic acid in beef, and how this increases with time when cattle are fed a grain-based diet. Oleic acid decreases the melting point of lipids from beef, increasing the perception of juiciness and improving beef flavor. Clinical trials have demonstrated that ground beef containing elevated oleic acid increases, or at the least has no negative effects on the concentration of HDL cholesterol. The amount of fat in published ground beef intervention trials greatly exceeds the amount of fat in equivalent portions of beef from U.S. domestic or Korean Hanwoo cattle. Thus, we conclude 1) Beef cattle should be raised under production conditions that increase the concentration of oleic acid in their edible tissues (i.e., by grain feeding over extended periods of time); and 2) The amount of fat consumed in a typical portion of beef will not increase risk factors for cardiovascular disease.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5018501/

Abstract

We know that animals are harmed in plant production. Unfortunately, though, we know very little about the scale of the problem. This matters for two reasons. First, we can’t decide how many resources to devote to the problem without a better sense of its scope. Second, this information shortage throws a wrench in arguments for veganism, since it’s always possible that a diet that contains animal products is complicit in fewer deaths than a diet that avoids them. In this paper, then, we have two aims: first, we want to collect and analyze all the available information about animal death associated with plant agriculture; second, we try to show just how difficult it’s to come up with a plausible estimate of how many animals are killed by plant agriculture, and not just because of a lack of empirical information. Additionally, we show that there are significant philosophical questions associated with interpreting the available data—questions such that different answers generate dramatically different estimates of the scope of the problem. Finally, we document current trends in plant agriculture that cause little or no collateral harm to animals, trends which suggest that field animal deaths are a historically contingent problem that in future may be reduced or eliminated altogether.

https://link.springer.com/article/10.1007/s10806-018-9733-8

Objective: There is suggestive data indicating a correlation among dietary protein intake and the progression of chronic kidney disease (CKD). Nonetheless, the exact associations between dietary protein intake and the incidence of CKD have remained uncertain. We performed the first meta-analysis to explore the correlation among total protein, plant protein, animal protein intake and CKD risk. 

https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2024.1408424/full

Lipolysis is the initial step in ketone body production, where triglycerides stored in adipose tissue are broken down into free fatty acids (FFAs) and glycerol.

This process is primarily stimulated by low insulin levels and high glucagon levels, which occur during fasting, prolonged exercise, or a low-carbohydrate diet.

Hormone-sensitive lipase (HSL), activated by β-adrenergic catecholamines and glucagon via the cAMP-PKA pathway, is a key enzyme in this process, catalyzing the hydrolysis of triglycerides to release FFAs.

The released FFAs are transported in the blood bound to albumin and taken up by the liver.

Once in the liver, FFAs undergo β-oxidation in the mitochondrial matrix, producing acetyl-CoA.

The availability of acetyl-CoA is the primary driver for ketogenesis, the process by which ketone bodies are synthesized.

The rate-limiting step in ketogenesis is the condensation of two acetyl-CoA molecules with one acetyl-CoA to form 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA), catalyzed by mitochondrial HMG-CoA synthase 2 (HMGCS2).

This step is highly regulated and can be activated by phosphorylation of HMGCS2 at Ser456 by protein kinase A (PKA) or casein kinase 2 (CK2), which occurs under ketogenic demand.

The HMG-CoA is then cleaved by HMG-CoA lyase (HL) to produce acetoacetate (AcAc), which can be reduced to β-hydroxybutyrate (βOHB).

The entire process is tightly regulated by hormones. Insulin inhibits lipolysis by suppressing HSL and activates acetyl-CoA carboxylase (ACC), leading to increased malonyl-CoA production. Malonyl-CoA inhibits carnitine palmitoyltransferase I (CPT1), the enzyme responsible for transporting fatty acids into the mitochondria for β-oxidation, thereby limiting the substrate available for ketogenesis.

Conversely, glucagon and other catabolic hormones like cortisol, epinephrine, and norepinephrine promote lipolysis and inhibit ACC, lowering malonyl-CoA levels and facilitating fatty acid entry into mitochondria, thus stimulating ketone body production.

The resulting increase in circulating ketone bodies, particularly βOHB and AcAc, serves as a crucial alternative fuel source for extrahepatic tissues, especially the brain, during periods of low glucose availability

People argue that agriculture helped us to develop civilizations, but it definitely hurt us from a health and developmental perspective. 

As to being able to run a civilization, that is not so convincing. The Native Americans in the Great Plains and elsewhere who were largely carnivores, if not completely carnivores in many areas, we're able to run a society with 100 million people living off of dried pemmican and fish. Genghis Khan and the Mongol horde took over the largest contiguous empire that has ever existed and they were carnivores as well, eating horse meat, drinking horse blood, and fermented mares milk. So you had one of the greatest civilizations and empires in the history of the known world eating meat from domestic stock and wild game and another massive civilization with multiple tribes and empires spanning most of the continent of North America doing the same. In fact, they found permanent buildings and what is now St Louis that could house 1 million full-time residents. This was found abandoned with the westward expansion after some sort of plague wiped out 95% of the population of North America. 

Lastly, there was a tribe in the Columbia River basin in Washington State who, because they had weirs and nets set up in the Columbia River with a massive salmon run, they had basically all of their time to themselves to devote to leisure activities as opposed to gathering food. If you calculate a civilizations wealth by the amount of leisure time they have compared to time they have to spend for basic necessities such as getting food etc, they are considered the wealthiest civilization that has ever existed. And yet no agriculture in this area at this time. 

So not only was agriculture one of the worst things that happened to us from a health perspective, it didn't give us the benefits of civilization that we have been told it did. 

https://www.doctorkiltz.com/fiber-myth/

Starting Nutrient Density week by defining what Nutrient Density Really Means...

Nutrient Density, Explained

At its core, nutrient density means how much life-sustaining nutrition is packed into each bite of food compared to the number of calories it carries.

High nutrient density = Foods that deliver a rich supply of vitamins, minerals, amino acids, and essential fatty acids in proportion to their energy. You don’t just get calories; you get building blocks for your brain, muscles, immune system, and every cell in your body.

Low nutrient density = Foods that are mostly starch, sugar, or processed fats. They may give quick energy, but they’re stripped of the vital compounds your body needs to repair, grow, and thrive. These are often called “empty calories.”

Why It Matters

1. True Satiety – Your body isn’t just looking for “fullness.” It’s searching for nutrients. If you fill up on empty calories, your stomach may be stretched, but your brain will keep sending hunger signals because the cells are still underfed.

2. Cellular Repair – Healing the brain, the gut, or the immune system depends on vitamins, minerals, and proteins that act as raw materials. Nutrient-dense foods provide these in concentrated amounts.

3. Metabolic Stability – When you eat nutrient-dense foods, blood sugar and hormones stabilize. When you eat nutrient-poor foods, your system swings between crashes and cravings.

4. Efficiency – With nutrient-dense foods, the body gets more out of less. You don’t need giant portions—you need the right portions of the right foods.

So in short: nutrient density means eating foods that not only fill the belly but truly fuel life—healing, energy, focus, and resilience.

The Nutrient Density Hierarchy

Tier 1: Most Nutrient-Dense (Animal Foods 🥩🐟🥚)

Beef liver → Vitamins A, B12, folate, iron, copper

Oysters → Zinc, B12, selenium

Egg yolks → Choline, vitamin D, healthy fats

Ribeye steak → Protein, iron, zinc, fat-soluble vitamins

Salmon (wild-caught) → Omega-3s (EPA/DHA), vitamin D, selenium

Bone marrow / broth → Collagen, glycine, minerals

👉 Dense, complete, and highly bioavailable — these foods build and repair the body.

Tier 2: Nutrient-Poor (Plant Foods 🥦🍎🌽)

Fruits → Mostly sugar + water, small amounts of vitamin C or potassium

Vegetables → Fiber + trace vitamins, but low density and often blocked by anti-nutrients (oxalates, phytates, lectins)

Grains & legumes → Some B vitamins, but poor absorption, missing essential amino acids, and often irritate the gut

👉 Not empty, but not dense. Missing essentials like B12, heme iron, complete protein, and bioavailable omega-3s.

Tier 3: Truly Empty (Processed Foods 🍩🥤🍟)

Sugary drinks, candy → Pure sugar, no nutrients

White bread, crackers, chips → Starch without meaningful vitamins/minerals

Seed oils → Calories without nutrition, inflammatory to the body

👉 Full stomach, starving cells.

⚡ Nutrient density isn’t about calories — it’s about nourishment.

https://youtu.be/Jeh3pkUBoW0?si=EcsFTsLvU-O-qwR4

The “Hateful 8” refers to the eight seed oils that do the most damage to human health. This is the research that the propaganda arm of seed oil manufacturers and pharmaceutical companies try to discredit with bought and paid for studies. Trillions of dollars in profits are tied to seed oils. Not just from manufacturers but pharmaceutical companies as well. They are fully aware of the harm seed oils do, it’s part of their business strategy. Create a demand for medicine to treat problems created by seed oils and other manufactured “food” like products. 

The hateful 8 research. 

https://drcate.com/pufa-project/

7 ways seed oils harm humans (selling non seed oil products)

https://repprovisions.com/blogs/rep-provisions-blog/7-reasons-seed-oils-are-bad-for-your-health

I’ve seen many posts recently lumping coconut oil in with all other plant oils, citing phytosterols replacing proper cholesterol and causing heart disease. 

There are very little phytosterols in coconut oil. That said you still shouldn’t cook with coconut oil since heating it will cause the formation of long chain polymers (liquid plastic). However, cold pressed coconut oil has health benefits. MCT oil made from coconut oil is very effective for boosting metabolism, reducing appetite and burning fat. 

Here’s a great study showing that coconut and coconut oil does not cause heart disease or atherosclerotic build up in the arteries.

https://pubmed.ncbi.nlm.nih.gov/7270479/

IF they cannot answer, find another doctor 

• How come life critical cholesterol, the precursor of hormones, is seen as bad

• How come 50% of heart attack victims have normal cholesterol

• Why does heart disease remain no. 1 killer despite massive statins, (it’s not working)

• How come the lower the cholesterol the higher the mortality -large RCT trials

Sometimes when your metabolism needs a reset, these products can be useful. I've used the first three successfully.

• MCT oil - 1 Oz 15 minutes before eating

• Apple Cider Vinegar (raw, unfiltered, unpasteurized with mother) - 1 Oz mixed in water 15 to 30 minutes before eating

• Forskolin extract - 1 capsule in the morning. Targets Visceral Fat. You can also take a capsule at night if required.

• Melatonin 250mg plus nightly

Dr. Ken D Berry, Family Doctor

Dr. Anthony Chaffee, Neurosurgion

Dr. Robert Kiltz, MD, Fertility Specialist

Dr. Timothy Noakes, MD, Diabetes

Dr. Shawn Baker, MD, Orthopedic Surgeon

Dr. David Diamond, MD, PhD researcher

Dr. Georgia Ede, MD, Alzheimer's & Dementia

Dr. Elizabeth Bright, MD

Dr. Robert H. Lustig, MD, Author

Dr. Annette Bosworth (Dr. Boz), MD