Using Fiber to Fight Cardiovascular Disease

Effects of Dietary Fiber and Statins on Serum Cholesterol Levels

Written by Belle Roberts

Cholesterol has a bad rap. Rather than being the villainous molecule the media makes it out to be, it’s actually essential to the structural integrity of our cells, a precursor for certain hormones, a vital component of vitamin D metabolism, and a precursor for bile acids. Our cholesterol content includes endogenous cholesterol, which the liver produces and recycles, and exogenous cholesterol that we intake through animal products.

When you intake fats, they’re converted and broken down into chylomicrons, which are taken into the blood by lacteals, vessels of the lymphatic system. These cholesterol-storing chylomicrons are then transported to the liver. Very-low-density lipoprotein, or VLDL cholesterol, is produced in the liver from endogenous triglycerides (the storage form of fats). VLDL circulates from the liver to the small intestine to interact with lipid absorption; 50% of this VLDL is returned to the liver, while the rest is converted to low-density lipoprotein (LDL) cholesterol, or “bad” cholesterol. 25% of that LDL enters non-hepatic tissues, which in excess can deposit in coronary walls. “Good” cholesterol, high-density lipoprotein (HDL) cholesterol, however, is transported from extrahepatic tissues to the liver. In short, cholesterol rotates through a cycle between the small intestine and liver, where it is stored and recycled into bile acids, which emulsify fats into smaller particles in order to be digested.

“Okay, where does fiber fit into this?” Shh, I’m getting there.

We hear a lot about “heart healthy” foods like Cheerios and rolled oats that help lower cholesterol levels, but the real reason these foods are helpful is their dietary fiber content. Fruits, veggies, nuts, and seeds are heart healthy too, they just don’t have a cartoon bee promoting them.

Dietary fiber is plant polysaccharides (complex carbohydrates) that are resistant to hydrolysis by digestive enzymes in humans. The power of fiber is that we cannot digest it. Soluble fiber, like that found in most fruits and vegetables, will undergo gel formation within the large intestine, increasing digestion and softening the consistency of a bowel movement. It can also bind directly to molecules or feed our colon microbiome (prebiotics are just soluble fiber pills). Insoluble fiber, found in grains, nuts, and seeds, increases fecal bulk and acts like a large intestine Zamboni, forcing undigested molecules out of the GI tract.

Fiber decreases serum cholesterol by decreasing bile acid recycling, cholesterol absorption, and cholesterol synthesis, as well as reducing insulin stimulation of cholesterol production.

Fiber binds to bile acids in the small intestine, pushing them out of the GI tract along with waste material; thus, forcing the liver to convert a stored cholesterol molecule into a new bile acid. Similarly, fiber can bind to cholesterol in the GI tract, forcing it out directly. Fiber also decreases cholesterol synthesis in two ways: generating propionic acid and slowing changes in blood glucose concentration. When the bacteria in our gut ferment dietary fiber, they convert it to lactate and short chain fatty acids. The short chain fatty acid propionate may inhibit cholesterol synthesis by entering the liver and inhibiting HMG-CoA reductase, the key regulatory enzyme in cholesterol formation. By controlling that enzyme’s activity, we are able to dramatically alter cholesterol synthesis. Insulin also stimulates HMG-CoA reductase. Gel formation of fiber in the gut decreases blood glucose response, which slows insulin activity; thereby, reducing stimulation of HMG-CoA reductase.

The dietary AI, or adequate intake, of fiber is 38g per day for men ages 19-50 and 25g per day for women ages 19-50. Not surprisingly, the average intake in the US is 17g per day and 13g per day for men and women, respectively.

It’s no wonder that cardiovascular disease accounts for 1 in every 4 deaths in the US.

The fat content of our blood is comprised of triglycerides and cholesterol. Healthy triglyceride levels hover under 150 mg/dL, while normal cholesterol levels lie under 200 mg/dL. High lipid levels increase risk of developing cardiovascular diseases, including atherosclerosis, heart attack, and stroke.

Atherosclerosis is especially prevalent in the western world and involves the accumulation of cholesterol in the arteries, the narrowing of the arteries, and the formation of abnormal surfaces in the arteries. There are general risk factors to developing atherosclerosis, like high blood pressure, cigarette smoking, and obesity; however biochemical risk factors include high LDL and low HDL cholesterol.

US corporate pharmacopeia has taken advantage of these risk factors by developing prescription drugs called statins, which inhibit HMG-CoA reductase. Its mechanism is targeted to the liver, but the disease-fighting effects rely on sufficient circulatory function; meaning prescription dosage must be increased to accommodate this. Statins rank number one among all prescribed drugs in the US, with Crestor selling nearly $5.6 billion worth of prescriptions inbetween July of 2013 and June of 2014. As of 2012, 28% of American adults over 40 reported taking a cholesterol-lowering medication in the past 30 days. Statins are incredibly effective at lowering serum cholesterol but require a lifelong commitment. Unlike fiber, which builds your intestinal resistance to cholesterol absorption and synthesis, statins work only when taking them as prescribed. Once you stop taking them, your cholesterol levels will shoot back up to unhealthy levels. However, statins and fiber can used symbiotically to maintain healthy lipid levels and gut function.

To sum up my ramblings for you, fiber elicits its effects via gel formation, binding to molecules, and fermentation by the gut microbiome. Statins lower endogenous cholesterol by inhibiting the key regulatory enzyme in cholesterol formation. Moreover, fiber and statins can be used together in disease prevention and management. Lipid levels can increase risk of diseases like atherosclerosis, diabetes mellitus, obesity, and gastrointestinal disorders like diverticulosis.

So stick it to the man -- eat your veggies.



Sources

https://www.mayoclinic.org/diseases-conditions/high-blood-cholesterol/in-depth/triglycerides/art-20048186

https://www.cdc.gov/heartdisease/facts.htm

https://www.youtube.com/watch?v=BRrB8Cxly9A

https://www.youtube.com/watch?v=U_4xM4zORN0

Brown, A. J. (2007), CHOLESTEROL, STATINS AND CANCER. Clinical and Experimental Pharmacology and Physiology, 34: 135-141. doi:10.1111/j.1440-1681.2007.04565.x

https://onlinelibrary-wiley-com.ezproxy.lib.calpoly.edu/doi/full/10.1111/j.1440-1681.2007.04565.x

Gropper, S., & Smith, J. (2013). Advanced nutrition and human metabolism (6th ed.). Belmont, CA: Wadsworth/Cengage Learning.

“Fat Burns in a Carbohydrate Fire”

Why the Keto Diet is Not As Great As Everyone Says it Is

Written by Belle Roberts

In a not-so-surprising revelation, I’ve found myself ruminating about how fad diet culture has yet to be expelled as of 2019. Probably the most notable and well-recognized diet is the Atkins Diet, now known as the ketogenic diet, which focuses on low carbohydrate and high fat and protein intake in order to produce a metabolic advantage. This advantage, however, is seemingly nonexistent.

In 1972, Robert Atkins published a wildly successful book, Dr. Atkins’ Diet Revolution, that was met with controversy. The general public gobbled up his writing, buying more than 15 million copies, while dietitians and other healthcare professionals were dubious of Atkins’ claims. His incredibly influential low-carb diet was based on a no-carbohydrate diet founded by Dr. Alfred Pennington during World War II. Pennington’s study was conducted using a small and non-representative sample of 20 DuPont University medical department executives, from which he concluded that a high-fat, high-protein, low-carb diet would prevent the body from turning too much food into fat. Although Pennington’s subjects lost a dramatic amount of weight, he doesn’t have the information and knowledge that we have now.

The world of nutrition and food science has come a long way in the last 75 years, but so much of the information that is constantly being pumped out by both researchers and the media can either be misinterpreted by the consumer or just incorrect from its origins. So how do we, as the general public, know what to trust? There’s probably a really complicated answer that I’m not qualified to give, but for now, let’s start off with this -- We don’t trust the keto diet.

The reason? Carbohydrates help burn fat. Fat burns in a carbohydrate fire -- that is, their metabolism is not exclusive, but integrated. This process of breaking down fats is called fatty-acid oxidation. Fat oxidation occurs in our cells’ mitochondria, where the Krebs cycle (an energy-conversion process), oxidizes a molecule called acetyl CoA to carbon dioxide, allowing our cells to harness energy from the food we eat. However, the Krebs cycle is dependent on glucose. If you don’t eat any carbs, you won’t be feeding your body any glucose. So what happens to this system without sufficient carbohydrate fuel? It becomes overwhelmed, causing acetyl CoA to accumulate and combine into ketone bodies. Granted, making ketones is totally normal; we’re all always making some ketones. The ketogenic diet, however, is forcing the body into ketosis, in which ketones accumulate and glucose depletes.

Without sufficient carbohydrate intake, the body will undergo gluconeogenesis (the conversion of amino acids, glycerol, and lactate to glucose) and hepatic glycogenolysis (the breakdown of glycogen to glucose in the liver) in order to maintain blood glucose levels. The amino acids used in gluconeogenesis are being stripped from skeletal muscle, essentially decreasing your lean body mass and negating your hard work in the gym.

“But, Belle,” you may say, “I’m eating a lot of protein, so that should give my body enough amino acids to deal with this.”

Unfortunately, that’s not how amino acid metabolism works. Amino acids, once broken down from the protein we eat, are dealt with immediately. They enter the liver, which basically degrades most amino acids to give us metabolic flexibility. Those that aren’t degraded are stored in skeletal muscle. There’s no way to take in a bunch of dietary protein to support gluconeogenesis.

When you have stopped feeding your body glucose for long enough that the liver doesn’t have any more stored in the form of glycogen, your cells will start to rely on ketones as an energy source. Ketosis will occur, in which ketones accumulate in the liver, enter the blood, and distribute among body tissues as an alternative fuel source. Meanwhile, gluconeogenesis is still occuring because: a) some cells, like red blood cells, can use only glucose as a fuel source, and b) glucose and ketones support each other.

Even though ketones work pretty well as an alternative fuel source, ketosis is metabolically expensive. It requires more overall energy to force the body to continue gluconeogenesis, as well as decreasing the density of skeletal muscle.

However, there are a lot of conflicting reports about the results of the keto diet. I hear this a lot: “But I have a friend who lost a lot of weight on the keto diet, and heard that people gain a lot of weight after they stop.”

That boils down to calorie deficit and water retention. The keto diet requires about 20-40 grams of carbs per day, verses the RDA of 130-150 grams per day (the brain and spinal cord consume 120 grams of glucose per day just by themselves). Such a massive difference is going to reflect what kind of carbs are consumed and what kind of foods are not eaten anymore at all. Fruits, vegetables, added sugars, and grains won’t really be in the diet anymore, so a person transitioning from a normal amount of carbs to the Atkins amount of carbs will probably also be eating fewer calories. Fruits and vegetables are good sources of electrolytes, which help draw water into tissues. Glycogen also increases tissue hydration, creating a new water flux in the body -- increasing with fruits, vegetables, and glucose sources, while decreasing in the absence of those carbohydrates. Being in ketosis will also lower the body’s BMR, or basal metabolic rate. Even if someone goes back to eating the same number of calories, but with a different macronutrient makeup, the body will struggle to adapt back to a higher BMR, increasing body fat percentage. Therein lies the dramatic weight loss and weight gain observed in the keto diet.

Studies like “Relatively High-Protein or Low-Carb Energy-Restricted Diets for Body Weight Loss and Body Weight Maintenance?” by Stijn Soenen, Alberto G.Bonomia, Sofie G.T. Lemmens, Jolande Scholte, Myriam A.M.A.Thijssen, Frank van Berkum, and Margriet S.Westerterp-Plantenga have shown that people who lose weight on a more carbohydrate-rich diet will have a higher chance of maintaining their goal weight compared to those on low-carbohydrate diets.

All in all, the keto diet is not recommended by healthcare professionals for a number of reasons. It saps your body of an efficient fuel source, as well as restricting the available sources of many important micronutrients and electrolytes. It’s a short-term solution to a long-term battle with weight loss.



Sources:

https://www.youtube.com/watch?v=lraWB2TgZ3M

https://www.nytimes.com/2003/04/18/nyregion/dr-robert-c-atkins-author-controversial-but-best-selling-diet-books-dead-72.html

https://www-sciencedirect-com.ezproxy.lib.calpoly.edu/science/article/pii/S0031938412002806

https://ac-els-cdn-com.ezproxy.lib.calpoly.edu/S2352396417302529/1-s2.0-S2352396417302529-main.pdf?_tid=b1c68d30-9f7b-4fee-900d-2545ddc1712f&acdnat=1548487573_973516e09feb2270d403aebf198fa9d6



Real Food Highlight: Jon Skirbina

Hey Foodie Friends! We are excited to debut our first post in a brand new blog series all about showing our appreciation for the amazing members of our food loving community.

This week our first addition of the Real Food Highlight series is all about Real Food Collaborative member Jon Skirbina!

Jon is a integral member of the Real Food Collaborative one of the current farm managers at the Cal Poly Organic Farm. The Real Food Collaborative would not be what it is today without him! He has full-heartedly offered his humble leadership, grounding support, and innovative ideas to our community and club. Not only has he served as president of the club and co-founder of the vegetable subscription program, but he has worked to secure meaningful and lasting relationships with campus partners such as the Cal Poly Organic Farm. We are so grateful to Jon for this program and the huge role he has taken up this year as the farm manager. He has given so much of his heart to this club and the seeds he planted are far reaching. He has been an anchor to our community over the last few years and the club would not be the same without him. We love you Jon! Thank you for growing our veggies, making us bread, and always making us laugh! This club wouldn’t be the same without you!

Below is a letter from Jon to the members of the Real Food Community:

Jon and his veggies!

Jon and his veggies!

Dear Real Food Collaborative community,

Yesterday was the first Veggie Pickup of the quarter. I was so excited that I got out of class early enough to participate in the delivery of purple sweet potatoes, tomatoes, basil and so many other beautiful veggies I had a literal hand in growing this summer. I sat on an unfurled blanket, talking with the coordinators of the Veg-Sitters, ooggling at a crazy sweet potato. I felt gratitude to all those involved.

Veg-Sitting has been extremely formative to my time at Cal Poly. In the early days it was three hours of unadulterated people-watching. Initially I would try to ensnare passersby with a welcoming “Hullo!” It usually only ensnared religious fanatics, or folks who were wondering “How much for 1 avocado?” Soon enough, I was seeing familiar faces and I could repeat the line “Everything here is pre-sold.” in my sleep. Regulars to Dexter included previous professors, transient students and a very polite evangelist. These characters afforded me new perspectives in the stillness. People literally passed me by as I sat still and watched, teaching myself to juggle tangerines (I still can’t). Soon, friends and club members with free time would gather (occasionally bribed with free oranges). Seeing subscribers every week was the best part, because each time I met them it reminded me why I was there, why I wanted to start the program.

Near the end of my first year here, the graduating president of the Real Food Collaborative, Jesse Gibson, asked me what real food the community should have access to. I told him that organic vegetables grown on campus should be sold on campus. He agreed and set off, with my naive support, to create a CSA. I don’t know how he really started the whole thing, I certainly helped, I think. At any rate, our pilot project was successful, but he was graduating. After the summer, the program would open up the the greater Cal Poly community. He would be handing the reins of a very strange looking horse to me. I cannot credit him enough as he badgered me to write an operations manual, set up a template for financial recording and do much more during that summer. Oh by the way, he said, you’re going to also be the president of the club this year.  I was nervous, but I came to Cal Poly because I wanted to feed people real food.

My dream for so long has been to build a food system alternative to the global industrial ones that seem so inescapable. And this is what I was doing. Somehow, I had connected with nearly 30 members of the community who wanted to participate in the very same thing. They also wanted food grown on the same land they lived on, they also wanted food grown by hand in fertile, living soil. These people became subscribers of the Veggie Subscription, many still remain loyal supporters. Over the first year the program peaked at nearly 40 subscribers. It was incredibly successful, the demand was there. Yet, I had a sort of tunnel vision about the project and the club. I was taking it more seriously than I should have, micromanaging everything.  I was exhausted and ready to give up.

I fled the country (took a quarter off for an internship). In the meantime, my good friends and peers in the Real Food Collab drastically improved RFC into what it is today: a network of foodies increasing access to real food to those who want it. They sought funding, built a website, delegated roles, and got me a job on the organic farm. I am truly honored to have been able to watch the veggie subscription evolve and grow, and happy to say that the program is now in  more and much better hands.

Though I can no longer veggie-sit for a full three hours every week, I am still so happy to join the current group of foodies who gather every Wednesday on Dexter. They are a part of an alternative localized food system that, to me, epitomizes real food. To have had a hand in the creation of this system is more than I could have hoped for in my time at Cal Poly. Growing roots and making space is so hard in a four-year university. Once the space is found and the seed is sprouted, you graduate, your projects end and you leave. I am now confident that this program will continue to succeed long after I graduate thanks to all of the allies, supporters, subscribers, coordinators, harvesters, veggie-sitters and eaters that have chosen to create this food chain. A seed planted, to be watered by others.

Genuinely,

Jon