Ketogenic Diet - Does the Type of Fat Matter?

Key Takeaways: 
  • Keto dates back to the 1920’s - it is a diet high in fat, and low in carbohydrates. It was found that three water-soluble compounds were made by the liver in response to food deprivation—acetone, β-hydroxybutyrate and acetoacetate, together called ketones, or ketone bodies. 
  • The type of fats you consume are really important to your health. In fact, it was found that a diet higher in polyunsaturated fats (PUFA) than in saturated fat induced a greater level of ketosis without adverse effect on lipid parameters.
  • The fast track to ketosis may be supplementation of PUFA which can be found mostly in nuts, seeds, fish, seed oils, and oysters as well as BodyBio Balance Oil and BodyBio PC.
America has embraced many diets and super foods to manage its obesity epidemic and to improve its quality of life, even hoping to address specific health problems. Lifestyle modifications recommended by physicians include dietary interventions, but most doctors know only what they were taught in a three-hour class in medical school. Their expertise in nutritional biochemistry needs fine tuning. The good news is that many are willing to do that. They might even go so far as to try motivational interviewing, goal setting or self-monitoring as viable techniques to help a patient practice weight management.  Energy deficit is typically needed to reduce weight, making calorie reduction a goal. Here, a low-carbohydrate diet might just be the ticket. Of course, it helps to be accompanied by at least a modicum of exercise.   

The History of the Ketogenic Diet 

The ketogenic diet has a long and varied history. It first popped up in the 1920’s through a faith healer who promoted fasting to help children with epilepsy, but was abandoned as soon as anticonvulsant drugs became available. It was successful at limiting—and even eliminating—seizures and became accepted therapy at the time. It was found that three water-soluble compounds were made by the liver in response to food deprivation—acetone, β-hydroxybutyrate and acetoacetate, together called ketones, or ketone bodies. This resulted from a diet high in fat and low in carbohydrates. The Mayo Clinic dubbed this the “ketogenic diet,” adopting it as epilepsy treatment about 1921. Later, in the 1960’s, the research found that more ketones are produced by medium-chain triglycerides (MCT’s) per unit of energy because they are carried to the liver through the portal vein, as opposed to the lymphatic system, allowing more protein and carbohydrate to be included in the diet, contrasted to the original ketogenic regimen. This made food more enjoyable for the patient. Besides maintaining ketosis, the diet is purported to strengthen athletic performance, to stabilize blood sugar, to burn fat, improve cognitive ability, and to suppress appetite.   

Ketones 

Of the ketone bodies in the blood, β-hydroxybutyrate is the most abundant, accounting for about 78%.  Acetoacetate makes about 20% and acetone a paltry 2%. Both β-hydroxybutyrate (BHB) and acetone are derived from acetoacetate (AcAc), with BHB the main one used for energy because of its abundance and stability.  Acetone is lost through respiration and sweat. Further, there are two kinds of BHB: the D- form used for efficient energy manufacture plus ancillary anti-ageing effects, and the L-form that helps to synthesize fatty acids (there’s more to this than there is room to explain it right now).    

So, how do you do this diet?

In a very low carbohydrate diet, the controlled production of ketone bodies causes a harmless physiological state known as dietary ketosis.  These ketone bodies move from the liver to extrahepatic tissue for use as fuel. Being able to cross the blood-brain barrier, they provide the brain with more than 70% of its energy (White, 2011).  Here, the brain notices the deficit of glucose and becomes receptive to ketone bodies (Pan, 2002). This quick absorption improves brain function by preserving the integrity of neurons and synapses, by allowing fewer free radicals, by decreasing neuro-inflammation (thus lowering risk of dementia), by reducing the possibility of depression and by improving cognition in people with dementia (Veech, 2017).   Wow! And research agrees that a very-low-carbohydrate diet causes a significant reduction in fat mass, with concomitant increase in lean body mass (Manninen, 2004). But all is not sunshine in the Emerald City.  

Does the type of fat in a ketogenic diet matter?  

There are only two from which to choose—saturated and polyunsaturated.  Yes, there is monounsaturated, but who’s going to swig a bottle of olive oil?  Even with canola oil—a disastrous choice because of its GMO background and very-long-chain fatty acids profile—an associated ketogenic regimen would probably require a liquid formulation.   A diet high in saturated fat likely would impair insulin sensitivity (Vessby, 2001) and have an adverse effect on lipid and lipoprotein metabolism with concurrent risk of vascular endangerment (Danke, 2001) (Hu, 2001).  That leaves PUFA. In fact, it was found that a diet higher in PUFA than in saturated fat induced a greater level of ketosis without adverse effect on lipid parameters (Fuehrlein, 2004).  

Ketogenic diet and weight loss

Low-carbohydrate, high-protein diets produce more dramatic weight loss than that attributed to a cut of 500 calories a day (which is supposed to cause a loss of one pound a week).   The initial weight loss in a keto diet comes from diuresis, not from a magical switch of metabolic activity. When carbohydrate is restricted, glycogen in muscle and liver are activated.  Each single gram of glycogen mobilizes two grams of water. In the liver, there is about a hundred grams of glycogen; in the muscles, about four times that. Bloating disappears soon after that mobilization of glycogen stores.  After all, a person will have lost almost a kilogram of excess baggage. What happens next is the generation of ketone bodies from catabolism of dietary and endogenous fat. Ketones are filtered by the kidneys as non-reabsorbable anions (Kolanowski, 1977), increasing distal sodium delivery to the lumen and thus renal sodium and water loss.  We hate to burst anyone’s bubble, but long-term weight loss might truthfully rely more on calorie restriction than on carbohydrate limitation.  After the diuretic phase passes, it becomes a matter of energy balance. Yes? No? Maybe? Most early studies—done in the 1980’s and 1990’s—have found zero statistical advantage to cutting carbs (Davie, 1982) (Piatti, 1993) (Rumpler, 1995) (Low, 1996) (Golay, 1996) (Golay, 1996). Worse, there are unexpected and inimical metabolic effects of a ketogenic diet.  Even in children there are concerns about dehydration, constipation and kidney stones.  Add to that hyperlipidemia, impairment of neutrophil function, optic neuropathy, osteoporosis and protein deficiency (Tallian, 1998).  Overzealous ingestion of saturated fat takes its toll on LDL cholesterol, especially if exercise and ancillary dietary interventions fall to the wayside.  Circulating free fatty acids may deterge cell membranes and interfere with ion channels, upsetting homeostasis (Henriksen, 2010). Removing some food groups from the diet may result in falling levels of calcium, magnesium, and iron.  Thiamine deficiency may arise. Biologically active phytochemicals from fruits and vegetables would be removed. Let’s not jump onto the bandwagon unless we know where it’s going. If you want to try the ketogenic diet, start slowly and pay attention to how you feel.

Can you fast-track Ketosis?

Controversy abounds in the mention of ketogenic diet. But not all people are created equal and neither are all keto diets. A strict ketogenic diet, can be too challenging and impossible to follow. We always encourage consumption of unprocessed organic food that is free of noxious oils, added sugars, and artificial elements. However, there is a way to assist your body in achieving ketosis without the strict limitation of carbohydrates.  Instead, ketosis can be rapidly achieved by introducing foods rich in essential fatty acids such as BodyBio Balance Oil and phosphatidylcholine, BodyBio PC, into the diet.  A diet that is organic, low-carb, and nutrient-dense; along with supportive lipids and other nutrients, will ensure that your body and cells are both cleansed and nourished.
Barzel US, Massey LK.  Excess dietary protein can adversely affect bone.  J Nutr. 1998 Jun;128(6):1051-3.   Davie M, Abraham RR, Godsland I, Moore P, Wynn V.  Effect of high and low-carbohydrate diets on nitrogen  balance during calorie restriction in obese subjects.  Int J Obes 1982; 6:457– 462.   Denke MA.  Metabolic effects of high-protein, low-carbohydrate diets.  Am J Cardiol. 2001 Jul 1;88(1):59-61.   Fuehrlein BS, Rutenberg MS, Silver JN, Warren MW, Theriaque DW, Duncan GE, Stacpoole PW, Brantly ML.  Differential metabolic effects of saturated versus polyunsaturated fats in ketogenic diets.  J Clin Endocrinol Metab. 2004 Apr;89(4):1641-5.   Garbow JR, Doherty JM, Schugar RC, Travers S, Weber ML, Wentz AE, Ezenwajiaku N, Cotter DG, Brunt EM, Crawford PA.  Hepatic steatosis, inflammation, and ER stress in mice maintained long term on a very low-carbohydrate ketogenic diet.  Am J Physiol Gastrointest Liver Physiol. 2011 Jun;300(6):G956-67.   Gershuni VM, Yan SL, Medici V.  Nutritional Ketosis for Weight Management and Reversal of Metabolic Syndrome.  Curr Nutr Rep. 2018 Sep;7(3):97-106.   Golay  A, Eigenheer  C, Morel Y, Kujawski  P, Lehmann T, de Tonnac  N. Weight-loss with low or high carbohydrate diet?  Int J Obes Rel Metab Disord. 1996; 20: 1067-1072   Golay  A, Allaz  AF, Morel Y,  de Tonnac N, Tankova  S, Reaven G. Similar weight loss with low- or high-carbohydrate diets.  Am J Clin Nutr 1996;63:174 –178.   Henriksen JR, Andresen TL, Feldborg LN, Duelund L, Ipsen JH.  Understanding detergent effects on lipid membranes: a model study of lysolipids.  Biophys J. 2010 May 19;98(10):2199-205.   Hu FB, Manson JE, Willett WC.  Types of dietary fat and risk of coronary heart disease: a critical review. J Am Coll Nutr. 2001 Feb;20(1):5-19.   Kolanowski J.  On the mechanisms of fasting natriuresis and of carbohydrate-induced sodium retention.  Diabete Metab. 1977 Jun;3(2):131-43.   Kosinski C, Jornayvaz FR.  Effects of Ketogenic Diets on Cardiovascular Risk Factors: Evidence from Animal and Human Studies.  Nutrients. 2017 May 19;9(5). pii: E517.   Low CC, Grossman EB, Gumbiner B.  Potentiation of effects of weight loss by monounsaturated fatty acids in obese NIDDM patients.  Diabetes1996; 45:569 –575.   Manninen AH.  Metabolic effects of the very-low-carbohydrate diets: misunderstood "villains" of human metabolism.  J Int Soc Sports Nutr. 2004 Dec 31;1(2):7-11.   McDonald TJW, Cervenka MC.  Ketogenic Diets for Adult Neurological Disorders.  Neurotherapeutics. 2018 Oct;15(4):1018-1031.   Pan JW, de Graaf RA, Petersen KF, Shulman GI, Hetherington HP, Rothman DL.  <2,4-13 C2 >-beta-Hydroxybutyrate metabolism in human brain. J Cereb Blood Flow Metab. 2002 Jul;22(7):890-8.   Piatti PM, Pontiroli AE.  Insulin sensitivity and lipid levels in obese subjects after slimming diets with different complex and simple carbohydrate content.  IntJ Obes1993; 17:375–381.    Rumpler WV, Seale JL.  Energy intake restriction and diet composition effects on energy expenditure in men.  Am J Clin Nutr 1995; 53:430 – 436.   Schugar RC, Crawford PA.  Low-carbohydrate ketogenic diets, glucose homeostasis, and nonalcoholic fatty liver disease.  Curr Opin Clin Nutr Metab Care. 2012 Jul;15(4):374-80.   Tallian KB, Nahata MC, Tsao CY.  Role of the ketogenic diet in children with intractable seizures.  Ann Pharmacother. 1998 Mar;32(3):349-61.   Richard L. Veech, Patrick C. Bradshaw, Kieran Clarke, William Curtis, Robert Pawlosky, M. Todd King.Critical ReviewKetone Bodies Mimic the Life Span ExtendingProperties of Caloric Restriction.  International Union of Biochemistry and Molecular Biology, 69(5):305–314, 2017 Vesely JM, DeMattia LG.  Obesity: dietary and lifestyle management.  FP Essent. 2014 Oct;425:11-5.   Vessby B, Uusitupa M, Hermansen K, Riccardi G, Rivellese AA, Tapsell LC, Nälsén C, Berglund L, Louheranta A, Rasmussen BM, Calvert GD, Maffetone A, Pedersen E, Gustafsson IB, Storlien LH; KANWU Study.  Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU Study. Diabetologia. 2001 Mar;44(3):312-9.   Walczyk T, Wick JY.  The Ketogenic Diet: Making a Comeback.  Consult Pharm. 2017 Jul 1;32(7):388-396.   Hayden White and Balasubramanian Venkatesh.  Clinical review: Ketones and brain injury. Crit Care. 2011; 15(2): 219.   Yi W, Xie X, Du M, Bu Y, Wu N, Yang H, Tian C, et al.  Green Tea Polyphenols Ameliorate the Early Renal Damage Induced by a High-Fat Diet via Ketogenesis/SIRT3 Pathway.  Oxid Med Cell Longev. 2017; 2017:9032792.    

Leave a comment

Please note, comments must be approved before they are published