Author: Dr. Stephen Fitzmeyer, Dr. Sharon Lojun

Keto vs GLP-1

Rethinking Cardiovascular Health: Beyond LDL as a Marker for Disease

Fellow physicians,

For decades, we’ve relied on LDL as the primary marker for assessing cardiovascular disease (CVD) risk. However, recent research and patient outcomes are prompting us to reconsider this approach. Cardiovascular health is multifaceted, and addressing root causes rather than singular markers like LDL can guide us to better patient outcomes, particularly in our current environment of rising metabolic and liver disease.

1. GLP-1 Medications: A Bridge, Not a Solution

While medications like Rybelsus (a GLP-1 receptor agonist) offer short-term weight-loss benefits, they come with limitations. Long-term use is costly and can bring side effects such as nausea, diarrhea, and gallbladder issues. Our patients may be drawn to the “quick fix,” but as we know, sustainable health often demands a lifestyle overhaul.

GLP-1s should be viewed as a temporary tool—a way to kick-start weight loss and motivate patients while emphasizing that lifestyle adjustments provide a sustainable path. Ideally, these medications serve as a bridge to instill healthier habits rather than a permanent solution.

2. The Real Culprit: Insulin Resistance and NAFLD

While elevated LDL is traditionally seen as a red flag for CVD, the underlying issue for many patients is actually insulin resistance. Insulin resistance is at the heart of metabolic syndrome, which drives non-alcoholic fatty liver disease (NAFLD)—a condition increasingly common, even among adolescents.

By focusing on insulin resistance rather than LDL alone, we tackle the metabolic issues that lead to NAFLD. Evidence shows that low-carb diets like keto can reverse fatty liver by lowering triglycerides and reducing liver fat, often leading to improved liver enzyme levels and overall liver health.

3. Better Metrics for Cardiovascular Health: TG/HDL Ratio and LDL Particle Size

Assessing cardiovascular risk requires a broader perspective. Rather than fixating on LDL, consider the triglyceride-to-HDL (TG/HDL) ratio—a stronger indicator of metabolic health. A lower TG/HDL ratio typically correlates with better heart health. Studies have shown that keto and low-carb diets improve this ratio by raising HDL and lowering triglycerides.

Additionally, while LDL levels may not change dramatically on a low-carb diet, LDL particles often shift to a larger, safer size, further reducing cardiovascular risk. These changes are more predictive of positive outcomes than LDL levels alone.

Moving Forward: An Integrated Approach to Patient Health

Incorporating GLP-1s can help patients get started, but it’s lifestyle modifications that will sustain them. Addressing insulin resistance with targeted lifestyle changes like low-carb eating can help reverse NAFLD, improve metabolic health, and reduce the risk of CVD.

Our role is to guide patients not only toward initial success but also to long-term, sustainable health. By shifting the focus from LDL to insulin resistance, we can empower them to achieve better outcomes and transform their health for the future.

  • header for salt

Exonerating Salt: Metabolic Syndrome Unveiled as the Underlying Culprit of Hypertension

By Stephen Fitzmeyer, MD

Introduction:
Hypertension, commonly known as high blood pressure, has long been associated with excessive salt intake. However, emerging research challenges this widely accepted belief, suggesting that hypertension is primarily a result of metabolic syndrome rather than a direct consequence of salt consumption. Metabolic syndrome, characterized by a cluster of metabolic abnormalities, including obesity, insulin resistance, and dyslipidemia, plays a pivotal role in salt retention and the development of hypertension. In this article, we will explore the misconceptions surrounding the salt hypothesis and delve into the intricate connection between metabolic syndrome and hypertension.

The Salt Paradox:
For decades, medical professionals and public health campaigns have emphasized reducing salt intake as a means to prevent and manage hypertension. However, the relationship between salt consumption and hypertension is not as straightforward as once believed. Numerous studies have failed to establish a consistent link between salt intake and blood pressure elevation. Furthermore, populations consuming low-salt diets have not demonstrated significant reductions in hypertension rates. This paradox raises questions about the true nature of the relationship between salt and hypertension.

Metabolic Syndrome: The Underlying Culprit:
Metabolic syndrome, a cluster of interconnected metabolic abnormalities, is now recognized as a significant contributor to hypertension. Obesity, insulin resistance, dyslipidemia, and chronic inflammation characteristic of metabolic syndrome disrupt the body’s delicate balance, leading to salt retention and the subsequent rise in blood pressure. Insulin resistance, a hallmark of metabolic syndrome, impairs sodium excretion by the kidneys, promoting salt retention and fluid accumulation. These metabolic derangements create a vicious cycle, perpetuating hypertension and further exacerbating the effects of salt retention.

Unveiling the Root Causes:
While salt intake may play a minor role in hypertension for a subset of individuals with salt sensitivity, it is crucial to focus on the underlying metabolic dysfunctions. Ultra-processed carbohydrates and fats, prevalent in modern diets, have been identified as primary culprits in the development of metabolic syndrome. These refined and heavily processed food products contribute to obesity, insulin resistance, and chronic inflammation, creating an environment conducive to hypertension and salt retention.

The Role of Lifestyle Interventions:
In addressing the underlying metabolic dysfunctions associated with hypertension, lifestyle interventions take center stage. A ketogenic diet, characterized by low carbohydrate intake and increased fat consumption, has shown promising results in improving metabolic health and blood pressure control. By shifting the body’s primary fuel source from carbohydrates to fats, a ketogenic diet improves insulin sensitivity, promotes weight loss, and mitigates chronic inflammation, thereby tackling the root causes of hypertension.

Intermittent fasting, an eating pattern that cycles between periods of fasting and feeding, has also demonstrated metabolic benefits. Beyond calorie restriction, intermittent fasting enhances insulin sensitivity, promotes autophagy, and regulates blood pressure, making it a valuable tool in the management of hypertension associated with metabolic syndrome.

Conclusion:
Contrary to the long-standing belief that salt intake is the primary driver of hypertension, the emerging evidence suggests that metabolic syndrome, with its associated metabolic dysfunctions, is the root cause of salt retention and subsequent development of hypertension. While salt sensitivity may play a role in some individuals, it is essential to address the broader metabolic context to effectively manage hypertension. Lifestyle interventions, such as adopting a ketogenic diet and incorporating intermittent fasting, offer promising strategies to reverse metabolic syndrome, improve metabolic health, and alleviate hypertension. By shifting the focus from salt intake to metabolic health, we can reframe our approach to hypertension management and pave the way for more effective prevention and treatment strategies.

Scroll to top