Ketogenic Diet: How Digestion affects Ketogenesis

How does the ketogenic diet affect digestion and how does digestion affect the results or symptoms you get from following the ketogenic diet?  Gut bacteria regulate gene expression of genes involved in glucose and fat absorption, and digestion determines what bacteria resides more permanently in our gut.  The more antibiotics you’ve consumed over your lifetime, the more resistant bacteria you’ll have with permanent changes in the genetic structure of bacteria.  This can give rise to conditions such as SIBO (Small Intestinal Bacterial Overgrowth) which is mentioned further down.


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Bile produced by the liver is responsible for the emulsification of fats and absorption from the digestive system into the bloodstream.  Interestingly enough cholesterol makes up part of the bile which is the very thing needed for cholesterol absorption.  To be more specific it is the combination of cholesterol, phospholipids and bile salts that make-up bile, and phospholipid synthesis is determined by healthy methylation and SAMe production.

You may need to use bitters to stimulate gastric acid production if the stomach pH is too high as a high pH of the food bolus that leaves the stomach and enters the small intestine will fail to trigger the gallbladder into releasing bile.

If you’ve had your gallbladder removed you will already be at a disadvantage.  There will be no controlled release of bile into the duodenum, but more of a constant dripping from the bile duct.  In this case you may have to use bile salts or digestive enzymes containing ox bile or pancreatic lipase.  It may also be useful to consume smaller amounts of fats stretched out over a longer period of time.  Because increasing fats will result in more bile dripping into the duodenum it is important to make sure the small intestinal lining is protected with high antioxidants.  This may include turmeric, green tea, resveratrol or any other polyphenols.  The reason behind this is that bile salts can be very corrosive to the gut wall and if there is constant contact of bile to the mucosa (as seen with gallbladder removal) this may predispose to duodenal cancer.  Just something to be aware of.



In general the ketogenic diet is great to starve dysbiotic bacteria and yeasts in the small intestine as found in conditions such as SIBO.  The low carbohydrate/sugar/fodmap diet will starve them of food and the high fat portion will stimulate bile production which will kill off pathogens and provide a better intestinal pH environment for the rest of the gut.

However, keep in mind that this may also increase die-off symptoms in those with severe overgrowth.  Gut dysbiosis may also be part of a bigger inflammatory process in the body which can increase PLA2 that breaks down cell membranes.  This is a problem because when cell membranes are damaged, insulin receptors and translocation proteins such as GLUT receptors also get damaged which greatly influences glucose transport into the cells and can sabotage the best designed ketogenic diets.

Also make sure you consume some fibre or prebiotics to feed bacteria in the large intestine so you don’t lose microbiome diversity.  Bacteria need fibre to grow and keep the digestive system healthy and functional.  There’s some discussion regarding ketogenic fibre which I’m not familiar with, but I suggest you read Ketogenic Fibre if you are curious.  Maintaining biodiversity in the large intestine is very important on a ketogenic diet.  Studies have shown that high fat diets where the microbiome shrinks are linked with bacteria producing LPS (lipopolysaccharides) that cause leaky gut, inflammation and obesity as part of metabolic syndrome.  Notice that I say ‘high fat diets’ and not ketogenic diets.  True ketogenic diets are low in sugars and carbs, so feeding of LPS-producing organisms is highly unlikely.  But it brings home the point that if you’re going to follow a ketogenic diet you need do it correctly.



Blood sugar levels will generally be higher during infection or with gut dysbiosis.  This is mainly because infection acts as a stressor in the body, stimulating HPA sympathetic activation, ACTH and cortisol release, and thus gluconeogenesis.  The process of gluconeogenesis changes amino acids from the diet into glucose, pushing blood sugar levels up.  Glucose absorption from the small intestine is also increased during infection.  This can be a big factor why some struggle to get into ketosis.



Also called ‘Keto Flu’ it is common to experience some symptoms in the early adaptation stages as the body shifts to a different fuelling system and release toxins.  Chemicals, hormones, metals, POP’s and many other toxins are trapped in fat cells.  As you get into ketosis and burn off more fat these substances are released back into the bloodstream for excretion through the liver and kidneys in stool and urine, even through sweating from the skin.  These organs need to be functional and able to remove these from the body.  How you cope with this will depend on how many toxins you’ve accumulated over your lifetime, how well your methylation works, how efficient your liver and kidneys are at flushing them out, whether you are constipated or not, and if you have any genetic blocks brought on by medications you may be on, nutritional deficiencies or genetic snips.  Generally the more fat you carry, the more toxins you will also carry.

If you experience adverse reactions during ketosis such as skin rashes, headaches, fatigue, etc. this could be the reason.  You may want to go slower by increasing carbs, look at additional kidney and liver support, lymphatic drainage or increased soluble fibre close to meals to bind to toxins from bile and stop their reabsorption back into the liver.



Bile acids can be very corrosive.  When you increase the fat in your diet you will also be dumping more bile and bile salts into the duodenum (small intestine).  This can cause problems in those with an already inflamed gut wall such as those with ulcerative colitis or Helicobacter pylori infections.  You can certainly still go on the ketogenic diet as fats are very healing for the gut wall, but you may initially have to increase soluble or mucilaginous fibre intake close to meals to protect the gut wall.




ANGPTL4 (Angiopoietin-like 4) is also known as FIAF (Fasting-Induced Adipose Factor).  We’ll just call it FIAF for ease of explanation.  FIAF is found in fat and muscle cells, but also the intestines which we will focus on in this discussion.  FIAF helps to regulate how much fat can be absorbed into cells before it becomes cytotoxic or bad for the cells.  So it is an important regulatory mechanism when it functions well.  In the intestines FIAF inhibits pancreatic lipase acitivity, the pancreatic enzymes responsible for breaking down fat during digestion.

So, in the presence of a high fat diet, FIAF will be upregulated and reduce lipase enzyme activity, reduce fat digestion, reduce fat absorption, produce ‘fatty’ stools and stop the person from gaining weight.  In other words, you absorb the fat you need and the rest is excreted.  Bacteria that increased intestinal FIAF production include Enterococcus faecalis, Lactobacillus paracasei (F19), Lactobacillus rhamnosus GG (LGG) and Bifidobacterium lactis 12 (BB12).

When you consume a high fat diet and FIAF is not upregulated (because remember, it protects the cells against fat toxicity) via inhibition by LPS or bacteria that deregulate fat storage and lipid metabolism, it will result in excessive fat digestion, absorption, inflammation and obesity.

So in order to keep FIAF expression optimal you need microbe biodiversity (including the lactobacilli and bifidobacteria mentioned above), very little or no LPS-producing gut bacteria (Streptococcus is a common one) and proper methylation.  If you follow a ketogenic diet and you gain weight on it instead of losing weight, I would start looking here as the combination of increased fat and glucose absorption during infection can sabotage the best efforts.


If you need guidance in the treatment of this or any other condition, please make an appointment with one of our practitioners.

This article is for information purposes only.  Please refer to our Medical Disclaimer policy for more information.  The opinions expressed here represents the author’s and not necessarily those of Realize Health.  In addition, thoughts and opinions change from time to time due to updates in research and as a necessary consequence of having an open mind.  Views expressed in out-of-date posts may not be the same to those we hold today.



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The impact of infection on gluconeogenesis in the conscious dog.

Hepatitis C Virus Infection Promotes Hepatic Gluconeogenesis through an NS5A-Mediated, FoxO1-Dependent Pathway

Angptl4 serves as an endogenous inhibitor of intestinal lipid digestion

Decreased Fat Storage by Lactobacillus Paracasei Is Associated with Increased Levels of Angiopoietin-Like 4 Protein (ANGPTL4)

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Elizma Lambert

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