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Dr. Richard Maurer
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Metabolic Health 
& Living with Parkinson's

Dr. Richard Maurer
In this episode, Brent sits down with Dr. Richard Maurer, a naturopathic doctor and author of The Blood Code, a book about metabolic health. They discuss markers like A1C, LDL, HDL, triglycerides, and how these impact risks for conditions such as diabetes and heart disease. Dr. Maurer shares his personal journey of reversing prediabetes and provides actionable insights on diet, exercise, and maintaining a balance between endurance and weight training to optimize health. The conversation then shifts to Dr. Maurer’s approach to his Parkinson’s diagnosis. With a focus on information, community, and proactive measures, he details how he has adapted his lifestyle to slow the progression of this neurodegenerative disease. Hope you enjoy.

Transcript

Richard: I cried for about ten minutes and then it was a matter of, "Okay, I gotta figure out what I can do now." And I told my wife, "I'm not going to watch TV with you anymore. I'm not going to read the paper, because I'm going to do nothing but read about Parkinson's for the next four months."

Brent: Welcome to Death Clock. I am your host, Brent Franson. Today we speak with Doctor Richard Maurer. The conversation with Doctor Maurer is both informative and inspiring. Doctor Maurer has written a book about managing metabolic health, and we talk a lot about the markers that we should all be paying attention to. We first start with the markers that indicate risk for diabetes.

Brent: That's going to be A1C and blood glucose. Richard was pre-diabetic and brought his measures into the normal zone. We also hit on some of the markers we need to think about for heart disease: LDL, HDL, triglycerides, and how to think about our own risk for heart disease. The second half of the conversation is about Richard being diagnosed with Parkinson's disease a couple of years ago.

Brent: He's got a really inspiring approach to dealing with such a brutal diagnosis. He's a wonderful guest. Hope you enjoy.

Brent: Doctor Richard Maurer, welcome to the show.

Richard: Brent, it's a pleasure to be here. Thanks so much.

Brent: I'm looking forward to chatting with you. You are a naturopathic doctor, which I'd like to talk about to clarify what that means. You've written a book called The Blood Code about metabolic health and your experience with reversing type two diabetes. Then, somewhere along the way, you were diagnosed with Parkinson's and are dealing with that.

Brent: Before we dive in, can you give us a sense of your background?

Richard: I've been in practice as a naturopathic doc for the past 30 years here in Maine. Naturopathic medicine, at least in Maine, is a licensed medical profession. We have prescriptive authority for a number of medications. I prescribe hormones for people, and we can use vaccinations and antibiotics.

Richard: We're in an endemic area for Lyme disease, so every time we turn around, there's sometimes a reason we really need to use an antibiotic. As a naturopathic doc, it's a bit more on the primary care side of things, where we can cover several other bases of health care.

Richard: For my training, in 1989, I went out to Portland, Oregon. At the time, there were only two naturopathic medical schools in the country that had a licensable program accredited by the Department of Education, located in Seattle and Portland. No surprise that people on the East Coast weren't quite as familiar with it as people in King County.

Richard: In Seattle, Washington, a naturopathic physician is many people's primary care doc. Bringing that training back to Maine was kind of novel in 1994. We introduced and passed the first law to cover the practice of naturopathic medicine. About 15 to 20 years into that, I wanted to start scratching my own itch.

Richard: I wanted to go into metabolic health and specialize. For the past 15 years, probably 75 to 80% of my client base has been focused on diabetes, weight, thyroid, or some combination of those three.

Brent: When you say metabolic health, what do you mean? I feel like that's a term that gets used a lot, and people nod because they think they're supposed to know what it means, but it's in a gray area where most people might not really know. When you say metabolic health, what does that mean?

Richard: My concern is that most people think of metabolic health as something related to weight loss, assuming my job as the physician is to speed up someone's metabolism to equate to better health, better performance, or a better life. As you can hear by my tone, I don't believe that.

Richard: Most of the time it doesn't work that way. Metabolism in science just means a balance between anabolism and catabolism. Our body is always doing that biological dance of breaking things apart to generate energy, making complex materials simpler. At the same time, it takes simple materials like glucose and builds them into glycogen so we can perform better tomorrow.

Richard: The balance of building muscle, fat, tissues, and bone density are anabolic processes. Breaking those things down are catabolic processes—things we foster with intermittent fasting, carb-restricted diets, and extended exercise. People practicing endurance training will often train low and race high.

Richard: They want glucose depleted during training and then race with higher glucose intake. There are all sorts of hacks and strategies we play. To me, that umbrella of metabolic health covers how to balance the body to hit that sweet spot.

Richard: I don't want to break down too much or lose muscle mass, which is an omen of worse things to come. That is where weight loss becomes a daunting metric. If someone is overweight and needs to lose weight, great. But over age 65, when people lose weight, it's often not the tissue we want to lose.

Richard: It's often loss of muscle mass, brain volume, or bone density. So when I talk about metabolic health, I encourage people to look beyond weight to find markers for a healthy metabolism.

Brent: You had pre-diabetes and reversed it. What does that mean from an A1C perspective or fasting blood glucose level? Where were you, and what did you do to get to a better place?

Richard: I had pre-diabetic numbers. My mother was a type two diabetic at age 60. Her A1C was around 7.0, and her triglycerides were triple her HDL cholesterol. Her fasting morning blood sugar was in the 130 to 140 range. Her fasting insulin was not extremely high, sitting around 7 or 8.

Richard: I come from a family where the people who get high blood sugar aren't overweight. People look at me and say it's impossible for me to get pre-diabetes because I'm not overweight, forgetting that about 30% of people with type two diabetes are lean. We miss a third of diabetics if we keep fixating on obesity as the sole common factor.

Richard: Subsequent generations that develop type two diabetes tend to get it about 15 years younger than their parents. My mother got it at 60, and by the time I was around 41 or 42, my A1C was creeping up to 6.1 and my morning blood sugar was around 104.

Richard: Why was my average sugar drifting so high? At the time, I was eating sourdough bread and fruit daily. The only exercise I was doing was endurance training—running, biking, and swimming for triathlons. In your 40s, you realize running constantly is tough on the body.

Richard: Running and swimming are glycogenic exercises that rely upon glucose for fuel. That wasn't helping my glucose-insulin tolerance. My insulin was on the low side, so it wasn't as simple as going low-carb to correct everything.

Richard: I dramatically lowered carbs by reducing bread and cutting back fruit, which brought my blood sugar down a little. However, it really took cutting back on running and increasing weight training to make the difference.

Brent: Does running negatively affect blood sugar, or does it just fail to positively affect it?

Richard: For me, I think it was slightly negative. It's not negative for most people, but it wasn't positive and took up time. It was burning calories I wasn't replacing well, and it wasn't signaling my body to build muscle mass.

Brent: If you're running long distances and swimming without weight training, and you adopt a keto diet, is that going to impact blood sugar levels significantly?

Brent: You're saying that alone won't have a huge impact on blood sugar levels?

Richard: For me, gaining 10 pounds actually improved my blood sugar control. A larger muscle mass allowed my body to absorb glucose and store it as glycogen. It created a sink to store energy.

Richard: Think of muscles as sponges storing glucose and glycogen. My body fat didn't go up. Being on the leaner side, my fat tissue can only hold so much energy before it's no longer healthy.

Richard: It took weight training—low reps, big muscle groups like squats—which naturally release testosterone. Weightlifting changed my body composition enough that my insulin resistance improved.

Brent: What was your A1C after the weightlifting and diet changes? Did you drop running and swimming entirely or just add weightlifting?

Richard: I cut back running and swimming by 80% for a period. I'm running a little more now because it feels good for other reasons, but restructuring it was key.

Richard: If I did a heavy lifting session and tried to run the same day, my trainer would ask why I got in the way of the anabolic recovery window when the body rebuilds.

Richard: I was interfering with recovery by running.

Brent: With weight training, you break down muscle, and it rebuilds stronger. Exertion must be followed by rest for that cycle to complete.

Richard: That's right. Workouts are catabolic and stress the body, so a workout is only as good as the allowed recovery.

Brent: Where did you get your numbers down to? As someone with a family history of type two diabetes who was pre-diabetic, what is your target for A1C or fasting blood glucose?

Richard: 6.1 was as high as I got. My brother reached around 6.2 or 6.3. I am down between 5.5 and 5.7 now. Some people might hear that and think it's on the higher side of normal.

Richard: There is no evidence suggesting an A1C of 5.1 is healthier than 5.6. With the rise of CGMs, there's a trend toward assuming lower is always better.

Brent: Correct me if I'm wrong, but is 5.7 or 5.8 considered the threshold for pre-diabetes, spanning up to 6.5?

Richard: Correct. Labs often mark 5.7 to 6.4 as the pre-diabetic range. Having written a book about using lab tests to tailor diet and lifestyle, I don't always stick to strict reference ranges, but an A1C around 5.7 is a solid baseline target.

Richard: Risk increases at 5.8. People shouldn't necessarily strive to stay below 5.0; drops into the 60s for blood sugar can indicate overly catabolic states. I often see patients with A1C levels at 4.7 to 4.9 coming in with migraines, low energy, and mood swings.

Richard: The idea that everyone needs to be at 5.0 or 5.1 isn't accurate.

Brent: So 5.2 to 5.7 is the sweet spot, 5.7 to 6.4 is pre-diabetes, and 6.5+ indicates type two diabetes. The pre-diabetic category serves as a clear warning zone, which isn't always present for other metrics.

Richard: Absolutely. I dislike the term "prediabetes" because it makes development sound inevitable, similar to calling a skin spot precancerous when the progression risk is relatively low.

Richard: Many pre-diabetic cases never turn into diabetes. However, remaining in the pre-diabetic range raises the risk of developing atherosclerosis by about 70%.

Richard: So even if it never becomes diabetes, it carries its own risks for overall mortality.

Brent: Building muscle helps store and process glucose better. What does your current diet look like? Have you optimized it? Is it keto, or do you still eat desserts, pasta, bread, or pizza?

Brent: Tell me about your typical daily diet.

Richard: I am not strict keto. I exercise a couple of hours a day, so I need carbohydrate boosts at times, which I tend to eat in the evening. My breakfast rarely exceeds 20 or 30 grams of carbohydrates.

Richard: My lunch rarely includes bread. Today, it was roasted delicata squash, a few slivers of potato, leftover steak, and a large salad with pomegranate seeds. I didn't avoid potatoes entirely, but lunch totaled under 30 grams of carbs.

Richard: Given my activity level, I eat more carbs at dinner to keep my blood sugar numbers optimized. Running worked well in my 20s and 30s, but now in my late 50s, weightlifting is necessary to maintain muscle mass for optimal health.

Richard: Looking at Alzheimer's prevention studies, exercise substantially improves risk profiles for dementia and neurological diseases.

Richard: A big component of that protective benefit comes from weightlifting.

Brent: So you aren't completely carb-free, but carb-light.

Richard: Yes. A "high carb" day for me is around 100 grams. In my book, The Blood Code, I suggest that people attempting to reverse type two diabetes restrict to 40 grams daily initially. That feels restrictive, like the 1970s Atkins approach.

Richard: As blood sugar stabilizes, people can increase to 60, 80, or 100 grams daily. Interestingly, the American Dietetic Association considers anything below 150 grams daily a low-carb diet.

Brent: What does 150 grams look like? For example, if I have a scoop of white rice at lunch, how many grams of carbs is that?

Richard: One cup of cooked white rice is about 40 grams. A slice of bread is 15 to 23 grams. A portion of fingerling potatoes is around 25 grams. If I order Thai takeout with duck and eat two cups of rice, that's 80 grams right there.

Richard: That pushes my carbs higher for the evening, alongside vegetables and duck.

Brent: Bryan Johnson talks about avoiding late-evening meals and carbs at night to optimize sleep. How do you view carb timing?

Richard: Studies on young men tested introducing casein protein at different times of day, including right at bedtime.

Richard: Timing didn't matter—adding protein combined with weightlifting built muscle and strength regardless of when it was consumed. The body acclimates to patterns fairly well.

Richard: Whether someone recommends eating carbs in the morning or backloading them at night, in the long run, the difference is negligible.

Brent: What does your sugar intake for pleasure look like? How often do you eat dessert, fruit, or sweet treats?

Richard: My main meals are low-carb, but we keep high-end gourmet ice cream at home. I'll occasionally enjoy a spoonful of that.

Brent: Doesn't fat content in ice cream process differently from pure sugar candy, blunting blood glucose spikes?

Richard: It just delays the peak. Both reach the same destination; one takes three seconds and the other takes nine seconds.

Brent: How should we think about HDL, LDL, and triglycerides in evaluating heart disease risk?

Richard: Let's look at triglycerides first. Triglycerides represent the anabolic storage of glucose transformed into fatty acid chains. These molecules store energy efficiently, taking up two and a half times less space than glycogen.

Richard: The body prefers storing energy as triglycerides for future use. Even on a keto diet, dietary fats like butter, cream, or egg yolks supply triglycerides directly without requiring conversion from glucose.

Richard: Triglyceride levels show residual stored energy and often correlate with body fat caliper measurements at the waistline. Optimal triglyceride levels range from 40 to 100 mg/dL.

Richard: Optimal triglycerides is 40 to 100.

Brent: So higher triglycerides mean more energy is being stored rather than used?

Richard: Yes. Circulating triglycerides represent an independent risk factor for arterial plaque deposition and atherosclerosis.

Brent: If unspent, those energy units can deposit in arteries and contribute to blockages.

Richard: Right, exactly.

Brent: What about the differences between HDL and LDL cholesterol?

Richard: Cholesterol is essential as a building block for sex and steroid hormones and for maintaining cell membrane repair. HDL is efficient at delivering cholesterol where needed and returning to the liver for recycling.

Richard: LDL carries stickier ApoB proteins, is prone to oxidation, and doesn't return to the liver as easily. While labeled "bad," the body deploys LDL to address localized inflammation and repair.

Richard: Chronically elevated levels increase plaque formation risks. Rather than relying on a one-size-fits-all approach of prescribing statins for high total cholesterol, checking actual arterial calcification is far more informative.

Richard: A coronary artery calcium (CAC) scan uses a brief CT scan to measure calcification across heart arteries directly.

Brent: That seems like an essential test for anyone over 40. It costs a couple hundred dollars out-of-pocket, takes 15 minutes, and provides clear visibility into arterial health.

Brent: It's non-invasive and straightforward to complete.

Richard: I paid $99 driving through Hartford, Connecticut. I did a podcast segment on it because it seemed too cheap to be true.

Richard: They ran a professional CAC scan, provided a DVD, and had a radiologist read it. You don't need to pay top dollar; some regional hospitals charge over $1,000 for the same test.

Brent: To recap: we want triglycerides under 100 mg/dL and a healthy ratio with HDL. How high should HDL ideally be?

Richard: If someone has genetic total cholesterol around 300, an HDL near 100 is ideal. Many women reach those numbers, but fewer men do due to genetic differences.

Richard: HDL should account for at least one-third of total cholesterol.

Brent: Where should LDL ideally be?

Richard: Standard guidelines flag anything over 100 mg/dL as elevated LDL, which flags almost everyone with total cholesterol over 190.

Brent: You sound skeptical of that blanket threshold.

Richard: There are many books challenging standard cholesterol myths. If a patient consistently shows 240 to 260 total cholesterol, I run a CAC scan if they are over 40.

Richard: I recently ordered one for a 36-year-old patient with an interesting family history, and his score came back significantly advanced.

Brent: The score measures calcium buildup via the coronary artery scan.

Richard: Exactly. The scoring is standardized across facilities. His left anterior descending artery showed a score around 246, which is high for a main coronary artery in a 36-year-old.

Brent: How do you interpret a case where someone has an LDL of 200, but a CAC score of zero?

Richard: A zero CAC score indicates no active plaque formation. They likely have low Lp(a) and a favorable ApoB/ApoA profile, which can be verified through advanced cardiovascular testing.

Richard: Direct-to-consumer lab testing platforms offer comprehensive cardiovascular panels for $200 to $300 that would otherwise cost thousands in a hospital setting.

Richard: Thousands.

Brent: How do you view medications? If a patient presents with high cholesterol, do you prescribe statins immediately?

Richard: I look for specific test results to tailor decisions for each individual. Standard protocols recommend 20 to 40 mg of atorvastatin for elevated cholesterol, or 80 mg plus aspirin following a cardiac event.

Richard: Following rigid flowcharts based strictly on raw lab numbers is not individualized medicine.

Brent: Switching topics: when were you diagnosed with Parkinson's, and what was that experience like?

Richard: Most people diagnosed can look back several years and spot early signs. I had an incident mountain biking in Wyoming where I passed out, fell, cracked my helmet, and lost consciousness for five minutes.

Richard: At the hospital, I told the ER physician that I passed out before falling rather than from a concussion. That orthostatic hypotension event was an early Parkinson's symptom.

Richard: A year later, while operating a log splitter, my hand got caught and I lost a fingertip, delaying my neurology appointment for a slight tremor.

Richard: Six months later, I sat down with a neurologist friend who estimated a 60/40 chance it was Parkinson's. I sought a second opinion in Boston, where the diagnosis was confirmed at 100%.

Richard: It took six months after the injury to finally see a neurologist.

Richard: He noted it looked like Parkinson's, which didn't fully settle in until I got home that evening.

Richard: When he gave me 60/40 odds, I traveled to Boston to get a definitive diagnosis from another neurologist.

Richard: At that point, the confirmation was 100%.

Brent: Is there a definitive blood test for Parkinson's?

Richard: At the time, diagnosis relied primarily on DaTscan imaging, which tracks dopamine transporter activity in the brain. In Parkinson's patients, loss of dopamine neurons results in diminished signal uptake on the scan.

Richard: The dye highlights active dopamine neurons, showing significant loss in Parkinson's cases.

Richard: Thanks to the Michael J. Fox Foundation, seed amplification assays using skin biopsies or spinal taps can now detect misfolded alpha-synuclein with over 90% accuracy.

Richard: This diagnostic test has only become widely available in the past nine months.

Brent: Is Parkinson's related to metabolic health, or is it a separate condition?

Richard: It is completely separate. I participated in genetic studies and reviewed my raw 23andMe data for LRRK2, PRKN, and other Parkinson's-related genes, but found no genetic markers.

Richard: About 85% of Parkinson's cases stem from environmental exposures triggering immune or neurotoxic responses, often linked to herbicides or industrial chemicals in water supplies.

Richard: As an autoimmune or neurotoxic reaction targets those compounds, dopamine-producing neurons sustain progressive damage. While disease progression cannot be stopped entirely, vigorous exercise has been shown to slow its advancement.

Brent: For 85% of cases, environmental factors play a primary role, unlike diabetes or dementia where lifestyle factors can be directly linked.

Richard: Cigarette smokers actually show lower rates of Parkinson's. The recent PD-NIC study evaluated whether nicotine patches slowed disease progression in newly diagnosed patients over two years.

Richard: The trial demonstrated that nicotine patches performed worse than placebo, ruling out isolated nicotine as the protective element.

Brent: So nicotine isolated does not help.

Richard: Exactly. Something else associated with smoking appears protective, confounding researchers looking for lifestyle links.

Richard: My 87-year-old mother has had an essential tremor for 40 years without significant progression. Children of individuals with essential tremors have a higher chance of developing tremors and double to triple the baseline risk for Parkinson's.

Richard: The book Ending Parkinson's Disease emphasizes advocacy, particularly banning agricultural chemicals like paraquat that correlate strongly with disease incidence.

Richard: You know, they say if you really want to get rid of Parkinson's, you've got to become an advocate. You know, getting at least paraquat, you know, one of those herbicides that's been used in the US to have excessive degree, you know, getting that off the market and out of our environment.

Brent: So herbicides represent a primary suspect currently?

Richard: Herbicides and trichloroethylene (TCE), a widely used industrial solvent. Growing up in New Jersey next to a 400-acre dairy and corn farm, our well water was likely exposed to heavy agricultural runoff.

Richard: The fields were heavily sprayed. When I moved to Maine near the former Brunswick Naval Air Station—now designated a Superfund site due to PFAS and TCE contamination—we relied on well water again. Those cumulative exposures 30 years prior likely contributed to my diagnosis.

Richard: Environmental exposures decades prior likely set the stage for my diagnosis.

Richard: Exposures decades prior ultimately manifested in disease onset.

Brent: What was your psychological process in coming to terms with the diagnosis?

Richard: I cried for ten minutes, then shifted focus toward taking action and connecting with support networks. Friends introduced me to the Davis Phinney Foundation in Boulder, Colorado.

Richard: I connected with Davis Phinney, a former pro cyclist diagnosed 30 years ago, and met the board chair of the Michael J. Fox Foundation nearby in Maine.

Richard: Those early connections were empowering. I told my wife I was spending the next four months immersing myself entirely in Parkinson's research, podcasts, and medical literature.

Richard: Information built empowerment, allowing me to make deliberate exercise and lifestyle choices to slow progression as much as possible.

Richard: I want to utilize every valuable tool available to manage my health proactive strategy.

Brent: That strategy includes an extensive exercise regimen of a couple of hours daily.

Richard: Yes. I transitioned away from triathlons toward social sports like paddle tennis, squash, dance classes, and pickleball.

Richard: Social engagement helps counter non-motor symptoms like fatigue and apathy. Beyond visible tremors, social connection remains vital.

Richard: I participate in Rock Steady Boxing and help organize rock climbing programs for Parkinson's patients in Maine.

Richard: Being surrounded by that community offers immense value.

Richard: The value of shared community experience is staggering.

Brent: In the community and connection.

Richard: In the community and connections, where mutual understanding exists without explanation. Early in the disease, I minimize dopamine medication to avoid side effects until necessary, focusing on long-term pacing.

Richard: Peter Attia talks about training for goals 25 years ahead. I remind 60-year-old patients that 60 to 90 is the same 30-year span as 25 to 55.

Richard: Design what a healthy 90 looks like at age 60 and work toward it, rather than focusing mournfully on what was lost.

Richard: Focusing on the future builds resilience against neurodegenerative decline.

Richard: Dwelling on past capabilities makes moving forward difficult with a progressive disease.

Richard: I measure success by making today excellent and building habits for my best self at 68.

Brent: I applaud your mindset—it reflects a remarkably healthy approach to a difficult condition.

Richard: Thank you. Even minor stress triggers tremors noticeably—speaking from the heart or experiencing emotional moments activates physical symptoms immediately.

Richard: When sitting with my adult children, expressing vulnerability causes noticeable physical shaking.

Richard: My daughter will gently encourage me to relax, and I remind them that visible tremors simply show when I am speaking sincerely from the heart.

Brent: You know.

Richard: If I'm not moving, it probably means I don't care that deeply about the topic.

Brent: Richard, I really appreciate you sharing your knowledge and wisdom from practice and lived experience. Thank you so much for joining us.

Richard: It's a pleasure to be here. I hope your community finds value in these insights. Lab numbers shouldn't be fixated on, but rather used to pivot and build habits that lead to your best future self.

Richard: Not to recreate a version of yourself from the past.

Brent: Well said. Thank you so much. Death Clock is recorded in Boulder, Colorado, produced by Patrick Gudino, with music by Patrick Lee, and hosted by Brent Franson, founder and CEO of Death Clock.

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