—Or, “The Alimentary Adventures of Ham & Swiss on Rye”
Ham and Swiss on rye is, well, one of the best things ever.
So we’ll use this sandwich to track the digestive system. In this digestive adventure, the sandwich will be our hero.
Warning: This post is a work-in-progress. I’ll continue to update it weekly, but for now, please excuse the mess.
A 30-second tour of the digestive system (aka the alimentary canal or GI tract)
Before we dive into more advanced stuff like hormones and neurotransmitters, let’s take a quick look at the organs involved in the digestive process.
In order, they are:
- Pharynx (throat)
- Small intestine
- Large intestine (colon)
Food travels through each of those. However, there are three other organs which play supporting roles in the digestive system:
There are three macronutrients, or “macros” for short: protein, carbohydrate, and fat.
- Ham = protein
- Rye bread = carbohydrate
- Swiss cheese = fat
Of course, each of those foods contain a blend of macros—for example, Swiss cheese has both fat and protein—but for the sake of simplicity, we’ll just use each food as one macro.
Each macro is made up of a smaller unit.
- Proteins are made up of amino acids.
- Carbohydrates are made up of monosaccharides, with the main one being glucose. (More on this in a second.)
- Fats are made up of fatty acids.
Let’s take a look at each.
First, we have monosaccharides (Latin for “one sugar”). The three are glucose, fructose, and galactose.
Carbohydrates are made up of saccharides (from the Latin for “sugar”). A complex carbohydrate has more saccharides are called polysaccharides (Latin for “many sugar”).
Oligosaccharides have some saccharides. The most frequent are disaccharides.
So what happens to our rye bread?
- In the mouth, salivary amylases break down the polys into smaller units.
- In the small intestine, pancreatic amylases break them down into maltose disaccharides.
- The maltose is broken down by the enzyme maltase, which yields two units of glucose.
- The glucose enters the body to be used for energy now, or to be stored for energy later as glycogen.
In addition, there are three types of polysaccharides:
- Fiber (indigestible; contains cellulose)
- Starch (exclusively glucose)
- Sugar (I think this is sucrose, which is glucose and fructose)
Disaccharides are made from a blend of monosaccharides. See below:
- Maltose = glucose + glucose
- Sucrose = glucose + fructose
- Lactose = galactose + glucose
Each disaccharide is hydrolyzed by a familiar-sounding enzyme. Thus, maltose is broken down by maltase, sucrose by sucrase, and lactose by lactase. Pretty simple, right?
Hormones and neurotransmitters in the digestive system—in order of appearance
I couldn’t find an order of which hormones and neurotransmitters occur where and when in the digestive process, so I pieced the following together myself. (This may or may not be correct.)
- Ghrelin is a hunger hormone that is released when you’re not eating enough. It stimulates appetite and the release of growth hormone.
- Gastrin (stomach). Produces gastric juice. Protein-rich foods tend to stimulate the most gastrin release.
- When hydrocholoric acid and pepsinogen are released in the stomach, the lower esophageal sphincter closes, peristalsis increases, the gallbladder contracts (to send bile to the small intestine), and the pancreas releases bicarbonate.
- Secretin (small intestine). Calls for bile and bicarbonate to neutralize acid. It inhibits gastrin. Released in response to hydrochloric acid.
- Cholecystokinin (CCK) asks the gallbladder to contract and release bile for emulsification of fats. It is released at the same time as secretin. Released in response to fat.
- Motilin (small intestine). Released when bicarbonate is dumped into the small intestine to neutralize stomach acid.
- Vasoactive intestinal peptide (VIP) slows down stomach activity while stimulating intestinal activity.
- Gastric inhibitory peptide (GIP). Small intestine. Decreases stomach churning to slow the stomach from emptying; stimulates insulin release; reduces gastric and intestinal motility; increases fluid and electrolyte secretion.
- Serotonin increases small intestinal motility and decreases the production of stomach acid.
- Once food (primarily fat) hits the end of the small intestine, neurotensin relaxes the lower esophageal sphincter, stops the production of stomach acid and peptin, and regulates motility. In other words, it closes up shop.
- Somatostatin: a hormone that inhibits the secretion of hormones—including glucagon, insulin, and gastrin.
- Peptide YY is released hours after eating. It inhibits stomach motility and tells the colon to absorb water and electrolytes (sodium and potassium).
- Acetylcholine is a “rest and digest” neurotransmitter that uses muscle contractions to move food through the GI.
- Overall, it takes about 4–8 hours for chyme to travel through the small intestine. It takes 12–25 hours to travel through the colon (large intestine) and out the anus.
- Useful video: https://www.youtube.com/watch?v=XANFAdMFkYY&ab_channel=AnatomyAcademy
- Wikipedia https://en.wikipedia.org/wiki/Gastrointestinal_hormone
Below is a table that summarizes the hormones and neurotransmitters.
|Motilin||Bicarbonate enters duodenum||Move chyme through intestines|
|Epinephrine||Fasting and/or exercise||Inhibit glycogen synthase|
Increase glycogen phosphorylase
|Norepinephrine||Fasting and/or exercise||Inhibit glycogen synthase|
Increase glycogen phosphorylase
|Glycogen synthase (enzyme, not a hormone!)||Turns glucose to glycogen|
|Glycogen phosphorylase enzyme||Breaks glucose off glycogen chain|
|Insulin||Glucose in bloodstream||Stores extra glucose in muscle and liver; also up-regulates glycogen synthase hormone|
|Neurotensin||When chyme enters the ileum||Relax the lower esophageal sphincter|
Stop production of stomach acid and bicarbonate
Glucagon and epinephrine both break down stored glycogen (a process called glycogenolysis)
A table of hormones (and enzymes) and how they affect each other
Hormones, like people, can turn each other on.
For example, insulin down-regulates growth hormone while up-regulating glycogen synthase.
Because of these relationships, I find it useful to think of hormones as “switches” that can be turned on or off. These switches are affected by other hormones.
Below is a table summarizing the relationships between hormones.
|Hormone 1||Hormone/enzyme 2|
|Somatostatin||inhibits glucagon, insulin, and gastrin|
|Insulin||activates lipoprotein lipase|
|Glucagon||activates hormone sensitive lipase|
|Epinephrine and norepinephrine||inhibits glycogen synthase|
The purpose of cellular respiration is to convert glucose—found predominantly in carbohydrates—into ATP.
But it’s not that simple. (Of course it isn’t. Nutrition is fucking hard!)
You see, there are three parts to cellular respiration:
- Glycolysis (also called the glycolytic pathway)
- The Krebs Cycle (or Citric Acid Cycle)
- Oxidative phosphorylation
Let’s start with glycolysis. It literally means “The splitting of glucose.” Glycolysis happens in the cytoplasm and is anaerobic. This process breaks down glucose in three ways: glucose in the bloodstream, stored glycogen, and glycerol (which was broken from a triglyceride).
In a nutshell, glycolysis converts glucose to pyruvate.
Between glycolysis and the Krebs cycle lies the transition reaction. This is where the pyruvate from glycolysis is converted to acetyl-CoA, which is the starting point for the Krebs cycle.
Transition reaction = Pyruvate (3 carbons) → acetyl-CoA (2 carbons) + CO2 + NADH.
Remember that each glucose molecule contains six carbons; therefore, each glucose molecule produces two molecules of pyruvate, which is then converted into two acetyl-CoA, two CO2, and two NADH.
Glucose → 2 pyruvate → 2 acetyl-CoA + 2 CO2 + 2 NADH
Now, you may be wondering what NADH is. This is when NAD+—which acts as a hydrogen buffer—gains a hydrogen molecule and becomes NADH. (Hence the “H” in NADH.)
In order for glycolysis to continue, the NADH must give up its hydrogen. This is done in one of two ways: either the hydrogen is passed on to the Krebs cycle, or it is combined with pyruvate to form lactic acid. In either case, the NADH recycles back to NAD+ and glycolysis continues.
Keep in mind, however, that while glycolysis continues, it can only go so fast. It’s like a particular gear on a bicycle: no matter how hard you peddle, you can only go so fast before you need to switch gears. So, glycolysis hums along, producing 2 ATP with each cycle, but at some point, you’re going to need to switch gears.
The next gear is the Krebs cycle.
Now, let’s move on to the Krebs cycle. The pyruvate created during glycolysis turns into acetyl-CoA, which is the starting ingredient for the Krebs cycle.
The Krebs cycle consumes acetate (in the form of acetyl-CoA) and water, reduces NAD+ to NADH, and produces carbon dioxide.
What happens if you don’t eat carbs?
Your body adapts. Here’s how: Your body converts fatty acids into acetyl-CoA via process called beta oxidation. During beta oxidation, two carbons are sliced off the end of a long fatty acid. These carbons become acetyl-CoA.
Beta oxidation is all fine and dandy, mind you, but it creates a problem: the acetyl-CoA begins to build up. (Nerd alert: this is because there isn’t enough oxaloacetate to move the acetyl-CoA to the Krebs cycle.) As the acetyl-CoA builds up, your liver—that glorious superhero of the digestive system—converts the acetyl-CoA into ketone bodies.
Key point: The fatty acid synthase system adds two carbon units to a fatty acid chain. Beta oxidation removes two carbon units.
Takes acetyl-CoA and converts it into ATP. There are two parts of this: the Krebs cycle (also known as the Citric Acid cycle) and the electron transport chain. (Is that not the coolest name?)
This energy pathway uses acetyl-CoA—which was produced either from glycolysis (glucose/glycerol) or beta-oxidation (fatty acids)—to produce ATP.
How much ATP? Well. Hold on to yer hats. The Krebs cycle produces two ATP, same as glycolysis.
But the election transport chain? The exact number differs, but it’s somewhere in the neighborhood of a whopping 32 ATP. That’s an immense amount!
First, amino acids have their nitrogen removed (in a process called deamination).
Once the nitrogen has been stripped, amino acids are used for either non-protein products (e.g. glucose via gluconeogenesis, which is Greek for “make new glucose”) or its carbon skeleton (also called α-keto acid, which is pronounced “alpha”) is used in either glucose or fatty acid metabolic pathways.
- Resistant starch isn’t digested by humans, but it plays an important role in health. When these starches reach the colon, they provide food for bacteria, who convert the starch into short chain fatty acids (SCFAs). These SCFAs are either absorbed by our bodies or used to feed our bacteria. (This is a good thing!)
- Speaking of good things, here are the benefits of SCFAs in the colon
- Long story short: if you eat enough resistant starch, you have enough SCFAs—which leads to improved health.
- Bob’s Red Mill Potato Starch is an easy way to get more resistant starch. 1 tablespoon = 8 grams of resistant starch. Remember: you must eat it cold! Resistant starch breaks down when heated (but you can always chill it after cooking). For example, you can cook potatoes or rice, then cool them in the fridge before eating.
- Green bananas are also a great source of resistant starch. While they taste gummy on their own, you can blend them in a smoothie.
- If you’re in ketosis, don’t fret: since resistant starch is not raise blood sugar levels, it will not kick you out of ketosis.
Lipolysis (“splitting fat”)
Lipolysis occurs when you break a triglyceride into a glycerol and its fatty acids.
Lipolysis = Triglyceride → Glycerol + Fatty acids
Triglycerides don’t enter our cells very well. Therefore, they are broken down through lipolysis so the glycerol and fatty acids can pass the plasma membranes and enter the cell. Once inside, they are put back together as triglycerides.
Ketosis for smart people
Although the “keto diet” has become popular, it’s not widely understood by most people.
In short, the purpose of a keto “diet”—and I loathe to call it a diet—is to restrict carbohydrate intake below ~50g/day. Once below this level, your body begins to produce ketone bodies and you’re said to be in ketosis.
I certainly enjoy being in ketosis. I began experimenting with it in 2016 while training for a 50-mile ultramarathon. Ketosis’s appeal for long-distance runners is simple: by reducing carbs, you increase ketones, and can run farther without running out of glucose. While training for the ultra, I routinely ran trail marathons in a fasted state.
Ketosis is a metabolic state. It is a not a diet based on particular macros. Why? Because there are many ways to get into ketosis. For example:
Not sure if this is correct (from Gundry/Tom podcast) 30% of calories in goat and sheep cheese is MCT. (Cows do not produce MCT.) This helps uncouple mitochondria—meaning the mitochondria produces heat rather than ATP, which can be a sign of metabolic flexibility and longevity. This may be a contributing factor in the Blue Zones, where many people are sheep and goat herders.
Position stands—a short-cut to find reputable, evidence-based advice from leading experts
Search for “position stands” from reputable organizations. You’ll get a brief summary of their stand on a wide variety of issues. This is really helpful for getting a high-level view of a subject. For example, here’s the International Society of Sports Nutrition position stand on protein intake on exercise. And here’s a list of all the position stands from the ACSM. (You can search online for any organization’s position stands pretty easily.)
How to build muscle
- You must be in a caloric surplus
- Eat up to 1g/lb protein bodyweight
- Train every body part twice a week
- Get at least 10–20 sets per week per body part
- 5 reps at heavy will get you as strong as 10–12 reps at moderate and 20 reps with light. This assumes you train close to failure. (1–2 reps shy of failure.) Variety is good, but the bulk of your training should be between 8–15 reps. This is the sweet spot that allows you to get more reps in without too much fatigue.
- Rest between 90 seconds and three minutes.
A list of foods high in fiber (and relatively low in carbs)
What will will likely kill you—and how to avoid it
Below is a list of what kills the most people in the U.S. (and likely most developed nations):
Aim for 500mL of water 30 minutes before exercising, and 250mL for every 15 minutes of exercise. Sure, this is all well and good, but I used to run trail marathons in a fasted state with no water and felt fine. Then again, I was probably being dumb.
Over-hydration can be a problem. In his book Natural Born Heroes, Chris McDougall points out that while long-distance runners die occasionally from over-hydrating, no one ever died from dehydration.
My take? Drink a bit more than you think you need ahead of time. Then sip occasionally.
- Protein supplements. Be sure to look for ones that are NSF Certified for Sport. Here’s a link.
A 20-minute walk after eating will reduce your post-prandial glycemia by up to 30%. To put that into perspective, that’s twice as effective as metformin, the most widely prescribed medicine for blood sugar control.