Dad's report (Normal FBG 180-200):
...blood reading this am was 102 haven't seen that number in ages. BP down too. Have done potatoes for 3 days, also dropped a few pounds. plan to keep it up a few more days...
In part 3, we'll look at the route a glucose molecule takes from the dinner plate until it is stored in your body.
If I tried to explain "glucose" I'd probably get it mostly wrong. People spend their entire lives studying glucose and glucose metabolism. For the most part, when we discuss glucose, we are talking about the basic six-carbon sugar molecule found in most carbohydrates. From Wikipedia on glucose:
Glucose is a ubiquitous fuel in biology. It is used as an energy source in most organisms, from bacteria to humans, through either aerobic respiration, anaerobic respiration, or fermentation. Glucose is the human body's key source of energy, through aerobic respiration, providing about 3.75 kilocalories (16 kilojoules) of food energy per gram. Breakdown of carbohydrates (e.g. starch) yields mono- and disaccharides, most of which is glucose. Through glycolysis and later in the reactions of the citric acid cycle and oxidative phosphorylation, glucose is oxidized to eventually form CO2 and water, yielding energy mostly in the form of ATP. The insulin reaction, and other mechanisms, regulate the concentration of glucose in the blood.
Glucose supplies almost all the energy for the brain, so its availability influences psychological processes. When glucose is low, psychological processes requiring mental effort (e.g., self-control, effortful decision-making) are impaired.
I'm sure some ketogenic dieters will take issue with the wiki on glucose, but that's beside the point. I wish to discuss how glucose gets from food to blood. It's not even all that important that you know what glucose is, or does, just that it is part of human biology and that too much in our blood is bad.
We eat carbohydrates. Somewhere within the carbs are glucose molecules. In a piece of bread, the glucose is found in the wheat starch. In an apple, the glucose is found in the sugars present. Generally, glucose is tightly bound in the starch or sugar and must be liberated. This liberation begins when we start to chew the food. We have an enzyme called "amylase" in our digestive system that breaks the bonds to turn "carbs" into glucose that we can absorb into our bloodstream, again, Wiki on amylase:
An amylase is an enzyme that catalyses the hydrolysis of starch into sugars. Amylase is present in the saliva of humans and some other mammals, where it begins the chemical process of digestion. Foods that contain large amounts of starch but little sugar, such as rice and potatoes, may acquire a slightly sweet taste as they are chewed because amylase degrades some of their starch into sugar. The pancreas and salivary gland make amylase (alpha amylase) to hydrolyse dietary starch into disaccharides and trisaccharides which are converted by other enzymes to glucose to supply the body with energy. Plants and some bacteria also produce amylase. As diastase, amylase was the first enzyme to be discovered and isolated (by Anselme Payen in 1833). Specific amylase proteins are designated by different Greek letters. All amylases are glycoside hydrolases and act on α-1,4-glycosidic bonds.
From potato to belly, we use chewing and amylase enzymes to convert potato starch to glucose. Cooked potato, as you may know, breaks down much more easily than raw potato starch. Acids and digestive enzymes found in the stomach further degrade carbs into glucose, or at least make them more available to enzymes injected into the small intestine by the pancreas. At any rate, most of the available glucose from the foods we eat is available for absorption into the bloodstream soon after it enters the small intestine.
How glucose gets from the small intestine to the blood stream has been debated for many years. There are two schools of thought. The traditionally taught pathway is via the cells which line the small intestine (epithelial cells) another theory suggests that the glucose transport occurs via the tight junctions.
The traditional view is that glucose is absorbed into the epithelium via a process known as active transport. Inside the cells which line the small intestine are a family of glucose transporters called sodium-glucose linked transporters (SGLT) proteins and glucose transporter (GLUT) proteins. This transportation system to move glucose out of the small intestine is a two-stage process that relies on glucose being absorbed into the intestinal epithelial cells via the SGLT and GLUT through a membrane. Then once inside the cells, being exported to the surrounding blood supply. Different sets of transport proteins orchestrate this movement through the cells until the glucose appears on the outside of the small intestine. See: Transport across Epithelia for more detailed information. Graphically, active transport can be drawn like this:
This same type of transportation mechanism is seen in the kidneys and throughout the body where a separation must be kept, i.e. blood brain barrier. There is another, somewhat controversial mechanism of glucose transport involving tight junctions.
Pappenheimer Hypothesis (Passive Transport)
This hypothesis states that "a major portion of intestinal glucose absorption occurs through tight junctions and not by saturable transcellular active transport." The link is to an abstract, I could not get the full text. But there are several papers focused on passive transport of glucose. Structural and Functional Analysis of Glucose Absorption Mechanisms in the Rat Small Intestine in vivo (full text), shows that glucose can be transported across TJs. Intestinal sugar transport describes several alternate glucose absorption pathways, including the Pappenheimer hypothesis, concluding (Drozdowsk and Thomson, 2006):
The process of intestinal sugar absorption remains a controversial topic.An increased understanding of this process will enable the development of better therapeutic strategies in conditions where the modulation of intestinal sugar transport could improve health. For example, reducing sugar absorption may be beneficial with regards to the treatment of diabetes or obesity.
I think Drozdowsk and Thomson nailed it, but why has this not been explored further? They have two citations for this paragraph:
Some studies have suggested that the “passive” component played a large role in glucose transport at high glucose concentrations, in some models contributing 3-5 times as much as the active component.
- Ilundain A , Lluch M, Ponz F. Kinetics of intestinal sugar transport, in vivo. Rev Esp Fisiol 1979; 35 : 359-366
- Lostao MP , Berjon A, Barber A, Ponz F. On the multiplicity of glucose analogues transport systems in rat intestine. Rev Esp Fisiol 1991; 47 : 209-216
It looks to me that passive absorption of glucose via tight junctions is a distinct possibility. We have also seen that tight junctions are prone to failure, especially in the presence of certain modern food additives.
I mentioned previously that the body has a mechanism in place to sense when to stop absorbing glucose into the blood. For healthy people, once the body's stores of glucose are filled and there is no more requirement, then transport of glucose from gut to blood will cease almost entirely.
Remember our old friend, leptin? When we eat, at some point the hormone leptin is secreted by fat cells and leads to several metabolic effects that make us stop eating. Much energy has gone into trying to develop pharmaceuticals and protocols to increase leptin production, availability, and sensitivity, but as far as I know, they all have been dismal failures (though some may disagree).
From Diverse roles of leptin in the gastrointestinal tract: Modulation of motility, absorption, growth, and inflammation (2010):
In physiologic states, leptin has been shown to decrease carbohydrate absorption by inhibiting d-glucose transport in the preprandial state and to upregulate glucose absorption in the postprandial state. Sodium–glucose transporter-1 is expressed in small and large intestinal mucosa and is responsible for absorption of glucose. Luminal and systemic administrations of leptin decrease the activity of this cotransporter through various mechanisms. It has been suggested that luminal leptin, most likely produced by gastric mucosa, rapidly decreases the expression and activity of sodium–glucose transporter-1 through a direct effect at the brush border...
Here is a mechanism described that interferes with active transportation of glucose across the gut-blood barrier we discussed earlier. Leptin is shown to turn off the SGLT transport system. There may be other feedback loops as well. The Role of Incretins in Glucose Homeostasis and Diabetes Treatment (2008) and Hormonal Signaling in the Gut (2014) both describe several other hormonal signalling systems that prevent glucose absorption into the blood via the epithelial cells and SGLT/GLUT proteins. Some of the hormones discussed are the "alphabet soup" that I describe in my book, The Potato Hack, ie, PYY, GLP-1, and CCK. These hunger hormones are very active when one embarks on the potato hack and serve to not only make us feel full, but prevent the importation of glucose from the small intestine at the appropriate times.
The Potato Hack Effect
When I first did the potato hack in 2012 or so, my fasting blood glucose (FBG) was quite high, 100-115 most days. I was eating a predominately low carb, somewhat ketogenic diet. The first morning of the all-potato diet and my FBG dropped to the 80's, then the 70's. It remained this low until I ended the hack. Upon resumption of my normal diet, my FBG returned to it's pre-hack level of 100+.
I've never quite been able to understand why the potato hack would lower an elevated FBG. I've heard many other people say the exact same thing, but not everyone. Also, this same effect is commonly reported by people who use raw potato starch as a prebiotic supplement, beans and oatmeal have a similar effect. There is a "Lentil Effect" described throughout the dieting world in which a meal heavy in lentils will reduce the post prandial blood glucose of the next meal. There are many theories why these reductions in FBG and PP BG occur, but I have yet to see anyone theorize that it is due to a tightening of a leaky gut.
Conclusion of Part 3
When eating an all-potato diet, you are performing the ultimate elimination diet. If there was a leakiness in the tight junctions, it should become apparent and your FBG or PP BG readings should rise. But the opposite occurs. My theory is that the potato hack, and many other high carb low fat diets must eliminate the the passive transport of glucose to the blood.
Is it possible that for many people who have diabetic or pre-diabetic levels of blood glucose that the problem is simply "leaky gut?" Removing ALL foods except potatoes quickly restores gut integrity and BG returns to normal levels despite eating massive amounts of easily digested glucose.
I'm not saying this is the case for every diabetic, and certainly there is insulin resistance after many years of high circulating glucose. In part 4 we'll look closer at glucose and discuss dietary strategy.
Also used: Regulation of Tight-Junction Permeability During Nutrient Absorption Across the Intestinal Epithelium