The following 9 tests are crucial for the diagnosis of metabolic syndrome, fatty liver, type 2 diabetes, and cardiovascular disease. A doctor must examine all of them for a proper and reliable diagnosis.

1. Abdominal fat

2. Triglycerides

3. HDL “good cholesterol”

4. Blood pressure

5. Fasting blood sugar (glucose)

6. Fasting insulin level

7. C-reactive protein (CRP)

8. Hemoglobin A1c

9. Homocysteine

What Is Metabolic Syndrome

The prevalence of metabolic syndrome worldwide has reached an epidemic dimension. Metabolic syndrome, or “insulin resistance syndrome” is a collection of five risk factors that precede the diagnosis of type 2 diabetes, cardiovascular disease, stroke, cancer, and neurodegenerative diseases. It is diagnosed when three of the following five markers are present.

Abdominal Fat

The easiest way to measure abdominal fat is the Waist-to-height ratio. Measure your waist circumference. Your waist circumference must be less than half your height. If your waist circumference is greater than half your height, you are overweight and insulin-resistant. That could indicate metabolic syndrome and a precursor to type 2 diabetes.

High Triglycerides

This is another fancy name for circulating fat in the bloodstream.

Normal: Less than 150 milligrams per deciliter (mg/dL), or less than 1.7 millimoles per liter (mmol/L)

Low HDL “Ggood Cholesterol”:

• Normal: Men greater than 40 mg/dL.

• Normal: Women greater than 50 mg/dL

High Blood Pressure

Normal —: Readings over 120/80mmHg and up to 130/85mmHg

Fasting Blood Glucose

Normal —: Less than 100 mg/dL (5.6 mmol/L). A fasting blood sugar level from 100 to 125 mg/dL (5.6 to 6.9 mmol/L) is considered prediabetes. If it’s 126 mg/dL (7 mmol/L) or higher on two separate tests, you have diabetes.

The Good News

All five symptoms have one single underlying cause, namely a high insulin level or in scientific terms, hyperinsulinemia, [1] which is a result of excessive intake of carbohydrates, sugar, and fructose. Let’s examine the link between hyperinsulinemia and each of these metabolic abnormalities before heading to four other markers.

Abdominal Obesity

The excess fat accumulation in the liver is decompressed and stored first in adipocytes (fat cells) followed by ectopic fat deposits, which means the fat within and around the abdominal organs. This is a clear indication of metabolic syndrome.

The underlying mechanism resulting in insulin resistance as well as the link between insulin resistance and abdominal obesity is already discussed in the chapters on fatty liver, fatty pancreas, and fatty muscles. If you want to review them, go ahead and read them again. What I am going to point out here is how to accurately classify abdominal obesity.

Why is conventional BMI, used by most GPs, not a reliable marker to show if someone is at risk of obesity and metabolic syndrome?

Many people have been classified as obese by BMI –, however, they are not. And the opposite is also true; there are lots of individuals who are missed by BMI to be classified as obese. This is well illustrated when someone has a standard BMI number, while with excess abdominal fat. BMI can't distinguish between fat and muscle, so it can tip more toned individuals into the overweight or obese categories, even if their body fat levels are in the healthy range. BMI is calculated without consideration of muscle mass, bone density, and total body composition, as well as race and gender differences. BMI also doesn’t take into account the whole-body fat percentage specifically the excess of visceral adipose tissue (ectopic fat deposition packed between internal organs), as an independent predictor of insulin resistance, type 2 diabetes, and cardiovascular disease.

Furthermore, liver insulin resistance is related only to the fatty acid levels in the liver, not the levels of visceral fat [2]. This may explain why many normal BMI individuals can have high levels of insulin resistance in the liver [3].

The latest scientific research shows that the most accurate predictor of both visceral fat and whole-body fat percentage (distribution of body fat) is the waist-to-height ratio (WHtR). [4] This is because of its high diagnostic precision and the exceptional simplicity of its determination.

High Ttriglyceride (Hhypertriglyceridemia)

I intend to demonstrate that too much sugar, and not dietary saturated fat, is the single root cause of high triglycerides, low HDL, and subsequent coronary heart disease. So far, studies have shown no significant association between dietary saturated fat intake and triglyceride levels. [5] And others have even found a reverse correlation. Triglycerides are made from substrate glucose and fructose by hepatic de novo lipogenesis (DNL), [6] which means generating new fat from glucose in the liver. Besides glucose, which most frequently provides carbon units for DNL, ​​fructose is an extremely lipogenic (fat-producing) substrate because it is solely metabolized by the liver, as I already explained in detail in Chapter Fatty Liver.

Excessive production of new fat in the liver eventually overstrains the export mechanism and leads to a retention of fat in the liver. The liver is full of fat. Due to the frequent consumption of refined carbohydrates and fructose, the glycogen level is also full. Besides that, there is readily available glucose in the blood that can be used for energy. In a situation like this, the liver sees no other option but to decompress itself by ripping apart the triglyceride into the blood (via VLDL), resulting in hypertriglyceridemia. Therefore, the levels of triglycerides in the blood depend on newly produced fat in the liver.

By lowering carbohydrate-sugar-fructose and eating fat, you entirely inhibit that mechanism. Why? Because there is no pathway between dietary fat and hepatic de novo lipogenesis. Dietary fat is taken up by chylomicrons (formed in the small intestine) and released into the lymphatic system, which is then emptied into the bloodstream without passing through the liver.

The Key Takeaway

When the liver glycogen is saturated and the supply of glucose is still abundant, insulin signals the liver to bank the excess glucose as fat. In simple words terms, it turns the sugar into fat and stores it. By eating fat, in contrast, you circumvent that pathway. Because there is no glucose, no insulin, and no new fat- production (de novo lipogenesis). As a result, our bodies shift to fatty acid oxidation, which means the breakdown of triglycerides for energy. This, in turn, inhibits hypertriglyceridemia, low HDL, and cardiovascular disease. Therefore, you want to shift your source of energy from sugar to fat.

Low HDL (“Good Cholesterol”)

HDL is beneficial to our health in multiple pathways. Here are just a few of them written super-simplified.

• It collects the used and excess cholesterols and transports them back to the liver for recycling.

• HDL neutralizes the harmful effects of pathogens (toxicities) and clears them from the body.

• Normal functioning HDL prevents the oxidation of LDL and subsequent inflammation.

• HDL interacts with the cells of the immune system to modulate the immune response

Increased triglyceride concentrations in the blood coincide with decreased levels of HDL. [7] High levels of triglycerides lead to low levels of HDL. Triglycerides activate the enzyme cholesterol ester transfer protein (CETP), which reduces HDL levels. Triglyceride enrichment of HDL by CETP enhances the clearance of HDL particles. [8] Low HDL is a component of metabolic syndrome, insulin resistance, hypertriglyceridemia, and hypertension.

The Key Takeaway

• A high level of triglyceride combined with low HDL indicates high LDL (“bad cholesterol”).

• A low-carb- hHigh-fFat diet lowers the triglycerides and raises the HDL.

• To increase HDL, also eat niacin (vitamin B3)- rich food such as egg yolk, grass-fed ground beef, turkey, chicken, liver, pork, and wild-caught fatty fish such as tuna, salmon, sardines, and anchovies.

High Blood Pressure (Hypertension)

The link between insulin and high blood pressure.:

1. As insulin concentration rises, both the percentage of the cardiac output and the volume of blood pumped by the heart elevates and is accompanied by an increased heart rate. [9]

2. Insulin also increases the volume of blood in circulation by magnifying the kidney’s ability to retain sodium. [10]

3. A high-fasting insulin level is an upstream common cause of too much production of uric acid by the liver [11]. Uric acid is an inhibitor of nitric oxide, which in turn promotes blood vessel elasticity and expansion. Nitric oxide also increases blood flow and decreases plaque growth and blood clotting [12]. In simple words, insulin decreases nitric oxide, resulting in blood vessel stiffness.

4. Another cause of stiffness of the blood vessels is calcification. [13] The Calcium deposits build up inside the wall of arteries to prevent the spreading of inflammations caused by too much glucose, toxins, heavy metals, and other inflammatory agents.

The Key Takeaway

The consumption of transfats and excess omega-6 fatty acids coming from hydrogenated vegetable oils and soybean oil causes your blood vessels to constrict. However, the omega-3 fatty acids widen your blood vessels and relieve inflammation of the arteries. [14] Eat food rich in omega-3 fatty acids such as egg yolk, grass-fed beef, New Zealand lamb, and wild-caught salmon.

Avoid these if you have hypertension:

• Refined carbohydrates, sugar, and high fructose corn syrup

• Stress and being constantly in fight-or-flight mode

• Heavy metals come mostly from farmed fish

• Trans fat and hydrogenated vegetable oils

• Anti-pregnancyContraceptive pills

• Excess caffeine

• Smoking

• Alcohol

High Blood Glucose

Insulin can maintain blood glucose in a normal range as long as the pancreas is not clogged in fat. It starts to become symptomatic when a fatty pancreas is not able to cope with the insulin production needed to regulate glucose. High blood glucose is the last symptom to appear before the diagnosis of type 2 diabetes.

There are two reasons why a blood sugar test is not reliable for diagnosing (pre-) type 2 diabetes.

• Fatty liver, which is caused by fructose, as explained here.

• Insulin hides the sugar as fat, which results in maintaining the blood sugar level in the normal range.

Therefore, ask your doctor to test for fatty liver and your fasting insulin level.

Here are four other essential Readings which need to be tested and Monitored by Your Doctor

Fasting Insulin Level

Your fasting insulin level is crucial for the diagnosis of pre-type 2 diabetes. Your blood sugar is in the normal range doesn’t mean you are not at risk of type 2 diabetes because the high level of insulin hides the excess sugar by forcing it into the cells and banking it as fat. Fasting insulin levels must be between 3-8 μIU/ml. Being greater than 8 μIU/mL is a sign of insulin resistance. Being greater than 12 μIU/mL shows severe insulin resistance.

C-reactive Protein (CRP)

is an inflammation marker. The ideal level ranges from 0.00 to 3.0 mg/L. CRP is produced by the liver and belongs to a group of proteins called acute phase reactants, which increase in response to inflammatory protein cytokines.

Hemoglobin A1c

A hemoglobin A1c (HbA1c) test measures the amount of glucose attached to hemoglobin, which tells you the average level of blood sugar over the past 3 months. For people without diabetes, the normal range for the hemoglobin A1c level is between 4% and 5.6%. Hemoglobin A1c levels between 5.7% and 6.4% mean you have a higher chance of getting diabetes. Levels of 6.5% or higher mean you have diabetes.

Homocysteine

A high homocysteine level (hyperhomocysteinemia) contributes to arterial damage. It makes a person more susceptible to endothelial injury, leading to inflammation in the arteries, which in turn results in blood clots, heart attacks, and strokes. [15] Hyperhomocysteinemia is an indication of a deficiency in vitamins B12 and B6, as well as folic acid. A normal level of homocysteine is less than 8 mcmol/L of blood. Increasing intake of folate, vitamin B6, and vitamin B12 decreases homocysteine levels. Therefore, to prevent a high homocysteine level and heart disease, eat beef, pork, eggs, poultry, organ meat, and salami.

Send me your questions.

I am here to help.

Scientific References

[1] Hyperinsulinemic syndrome: the metabolic syndrome is broader than you think. Kelly CT, Mansoor J, Dohm GL, Chapman WH 3rd, Pender JR 4th, Pories WJ. Surgery. 2014 Aug;156(2):405-11. doi: 10.1016/j.surg.2014.04.028. Epub 2014 Jun 21. Review. PMID: 24962189

[2] Fabbrini E, Magkos F, Mohammed BS, Pietka T, Abumrad NA, Patterson BW, et al. Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity. Proc Natl Acad Sci U S A. 2009;106(36):15430–15435. doi: 10.1073/pnas.0904944106.

[3] Azuma K, Kadowaki T, Cetinel C, Kadota A, El-Saed A, Kadowaki S, et al. Higher liver fat content among Japanese in Japan compared with non-Hispanic whites in the United States. Metabolism. 2009;58(8):1200–1207. doi: 10.1016/j.metabol.2009.03.021.

[4] Association of Waist Circumference and Body Fat Weight with Insulin Resistance in Male Subjects with Normal Body Mass Index and Normal Glucose Tolerance. Sasaki R, Yano Y, Yasuma T, Onishi Y, Suzuki T, Maruyama-Furuta N, Gabazza EC, Sumida Y, Takei Y Intern Med. 2016; 55(11):1425-32.

[5] Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: results of the OmniHeart randomized trial. Appel LJ, Sacks FM, Carey VJ, Obarzanek E, Swain JF, Miller ER 3rd, Conlin PR, Erlinger TP, Rosner BA, Laranjo NM, Charleston J, McCarron P, Bishop LM, OmniHeart Collaborative Research Group. JAMA. 2005 Nov 16; 294(19):2455-64.

[6] Softic S, Cohen DE, Kahn CR. Dig Dis Sci. 2016 May;61(5):1282-93. doi: 10.1007/s10620-016-4054-0. Epub 2016 Feb 8. Review. PMID: 26856717

[7] Pathophysiology of reverse cholesterol transport. Insights from inherited disorders of lipoprotein metabolism. Reichl D, Miller NE Arteriosclerosis. 1989 Nov-Dec; 9(6):785-97. Metabolic heterogeneity associated with high plasma triglyceride or low HDL cholesterol levels in men. Lamarche B, Després JP, Pouliot MC, Prud'’homme D, Moorjani S, Lupien PJ, Nadeau A, Tremblay A, Bouchard C Arterioscler Thromb. 1993 Jan; 13(1):33-40.

[8] Plasma cholesteryl ester transfer protein and high-density lipoproteins: new insights from molecular genetic studies. Tall AR J Intern Med. 1995 Jan; 237(1):5-12.Triglyceride enrichment of HDL enhances in vivo metabolic clearance of HDL apo A-I in healthy men Lamarche B, Uffelman KD, Carpentier A, Cohn JS, Steiner G, Barrett PH, Lewis GF. J Clin Invest. 1999 Apr;103(8):1191-9.

[9] Effect of insulin on the distribution of cardiac output in the fetal lamb. Milley JR. Pediatr Res. 1987 Aug;22(2):168-72. PMID: 3309856

[10] The inter-relationship between insulin resistance and hypertension. Salvetti A, Brogi G, Di Legge V, Bernini GP. Drugs. 1993;46 Suppl 2:149-59. Review. PMID: 7512468

[11] Correlation of the Serum Insulin and the Serum Uric Acid Levels with the Glycated Haemoglobin Levels in the Patients of Type 2 Diabetes Mellitus. Gill A, Kukreja S, Malhotra N, Chhabra N. J Clin Diagn Res. 2013 Jul;7(7):1295-7. doi: 10.7860/JCDR/2013/6017.3121. Epub 2013 May 11. PMID: 23998049

[12] Nitric oxide in hypertension. Hermann M, Flammer A, Lüscher TF. J Clin Hypertens (Greenwich). 2006 Dec;8(12 Suppl 4):17-29. Review. PMID: 17170603. Impaired endothelial nitric oxide bioavailability: a common link between aging, hypertension, and atherogenesis? Walsh T, Donnelly T, Lyons D. J Am Geriatr Soc. 2009 Jan;57(1):140-5. doi: 10.1111/j.1532-5415.2008.02051.x. Epub 2008 Nov 14. PMID: 19054194. Nitric oxide and arterial disease. Barbato JE, Tzeng E. J Vasc Surg. 2004 Jul;40(1):187-93. Review. PMID: 15218485.

[13] Gervais Muhire, M. Florencia lulita, Diane Vallerand, Jessica Youwakim, Maud Gratuze, Franck R. Petry, Emmanuel Plane!, Guylaine Ferland, and Helene Girouard. Originally published 6 May 2019 1 https://doi.org/10.1161/JAHA.118.0116301 Journal of the American Heart Association. 2019;8:e011630

[14] Fish oil supplementation, resting blood flow and markers of cellular metabolism during incremental exercise. Pearson SJ, Johnson T, Robins A. Int J Vitam Nutr Res. 2014;84(1-2):18-26. doi: 10.1024/0300-9831/a000189. PMID: 25835232. Omega-3 Fatty Acids and Inflammatory Processes Calder PC. Nutrients. 2010 Mar;2(3):355-74. doi: 10.3390/nu2030355. Epub 2010 Mar 18. Review. PMID: 22254027.

[15] Cattaneo, M (February 1999). "“Hyperhomocysteinemia, atherosclerosis and thrombosis"”. Thrombosis and Haemostasis. 81 (2): 165–76.