Blood lipids and risk factor for heart disease

1.      Effects of nutrients on blood fats

Blood lipids (or blood fats) are lipids in the blood, either free or bound to other molecules. They are mostly transported in a protein capsule, and the density of the lipids and type of protein determines the fate of the particle and its influence on metabolism. The concentration of blood lipids depends on intake and excretion from the intestine, and uptake and secretion from cells. Blood lipids are mainly fatty acids and cholesterol. Hyperlipidemia is the presence of elevated or abnormal levels of lipids and/or lipoproteins in the blood, and major risk factor for atherogenesis, cardiovascular disease [1].

The American Heart Association´s recently revised dietary guidelines advocate a population-wide limitation of saturated fat to 7% of energy, trans-fat < 1% of energy and cholesterol 200 mg/day to reduce the risk for CHD by choosing lean meats and vegetable alternatives, fat-free (skim) or low-fat (1% fat) dairy products and minimize intake of partially hydrogenated fats; minimize intake of beverages and foods with added sugars; choose and prepare foods with little or no salt [2]. Most saturated fats (SFA) of animal foods (meat and dairy) increase serum total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C); polyunsaturated fatty acids (PUFA) lower serum cholesterol concentrations [3]; and monounsaturated fats (MUFA) either lower [4] or have no influence on plasma TC or LDL-C [3]. Trans-fatty acids (stereo-isomers of the naturally occurring cis-linoleic acid) raise LDL-C; effects on inflammation have been conflicting [5]. Omega-3 fatty acids are PUFAs including eicosapentaenoic acid (EPA) and decosahexaenoic acid (DHA) in ocean fish and fish oils are associated with a decreased CVD [1].

Carbohydrate. Evidence for the paradoxical rise in serum lipid levels and fall in HDL levels is associated with consumption of a diet higher than usual in carbohydrates [1].

Fiber on fruits, vegetables, legumes, and whole grains is effects to lower LDL-C. In particular, the soluble fibers in pectins, gums, mucilages, algal polysaccharides, and some hemicelluloses lower LDL-C [1].

Antioxidants. Two dietary components that affect the oxidation potential of LDL cholesterol are the level of LA in the particle and the availability of antioxidants. Vitamin C, E, and vitamin A (β-carotene) at physiologic levels have antioxidants roles in the body and the most concentrated antioxidant carried on LDL-C to prevent risk factor for CVD [1].

Soy protein. Only very large intakes of soy protein may decrease LDL-C by a few percent when it replaces animal protein [6].

Stanols and sterols. Plant stanols and sterols isolated from soybean oils or pine tree oil have been known to lower blood cholesterol and LDL-C in adults [7].

2.      Diagnose of hyperlipideima

The main types of blood fats are:
Total cholesterol

      LDL-cholesterol is often called bad cholesterol
      HDL-cholesterol is often called good cholesterol
      Triglyceride (TG)

Diagnose

Do a simple sufficient blood test. Need to measure total cholesterol and HDL-cholesterol at any day and without fasting. Other blood fats are more sensitive to measurement and requires constant. In general, it advised that the person is fasting for > 6-12 hours of food lipids. TG measurement is sensitive to food intake within 12 hours [8].

What is need to measured and AHA (American heart association) recommendation

Cholesterol plays a major role in a person's heart health. High blood cholesterol is a major risk factor for coronary heart disease and stroke. They should also learn about their other risk factors for heart disease and stroke. Total blood cholesterol is the most common measurement of blood cholesterol. Cholesterol is measured in milligrams per deciliter or mmol per liter of blood (mg/dL or mmol/dL) [9].

The Third Report of the Expert panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III or ATP III) was released in 2001. It recommends that everyone age 20 and older have a fasting "lipoprotein profile" every five years. This test is done after a 9–12-hour fast without food, liquids or pills. It gives information about total cholesterol, low-density lipoprotein (LDL) or "bad" cholesterol, high-density lipoprotein (HDL) or "good" cholesterol and triglycerides (blood fats) [9].

Initial classification based on total cholesterol and HDL cholesterol

It is advisable to measure the basic factors that reflect on total blood fats. What is usually measured [8]:

Total cholesterol
- Optimal < 5.2 mmol/l
- borderline high 5.2-6.2 mmol/l = increased risk
-  High > 6.2 mmol/l = substantially increased risk. High blood cholesterol. A person with this level has more than twice the risk of coronary heart disease as someone whose cholesterol is below 6.2 mmol/l.

LDL-cholesterol
- Optimal < 2.6 mmol/l
- Near or above optimal 2.6-3.3 mmol/l
- Borderline high 3.4-4.1 mmol/l = increased risk
- High 4.1-4.9 mmol/l = substantially increased risk
- Very high 4.9 mmol/l = substantially increased risk

Triglycerides (TG)
- Normal < 1.7 mmol/l
- Increased 1.7-2.2 mmol/l = increased risk
- Significantly increased 2.2-5.6 mmol/l = substantially increased risk
- The heavy increase 5.6 mmol/l = substantially increased risk

HDL-cholesterol
- The low value of 1.0 mmol/l = substantially increased risk. Low HDL- cholesterol level. A major risk factor for heart disease.
- The average value of 1.0-1.6 mmol/l
- The high value of 1.6 mmol/l = protective effect. High HDL-cholesterol level. A HDL of 1.6 mmol/L and above is considered protective against heart disease.

3.      Cases

Calculators of LDL-cholesterol level from formula Friedewald and valuation of risk fators for cardiovascular diseases in cases on next 10 years.

LDL = total cholesterol - HDL - VLDL (=1/5 TG)

Case1: 60 years old man

-          Total cholesterol 7.8 mmol/L > 6.2: level has more than twice the risk of coronary heart disease.

-          HDL-cholesterol 0.9 mmol/L < 1.0: low HDL- cholesterol level. An increased risk factor for heart disease.

-          TG 2.5 mmol/L > 2.2: substantially increased risk

-          Calculated LDL = 7.8 - 0.9 - (2.5/5) = 6.4 mmol/L > 4.9: very high, substantially increased risk.

-          Limit of systolic blood pressure 125 mmHg

-          Risk factor: 21.4% compared with 6.5% of normal people or 3 folds higher risk for CVD than normal cases of same gender and age on next 10 years.

Case2: 67 years old woman

-          Total cholesterol 7.0 mmol/L > 6.2: level has more than twice the risk of coronary heart disease.

-          HDL-cholesterol 2.7 mmol/L < 1.6: High HDL cholesterol. An HDL of 1.6 mmol/L and above is considered protective against heart disease.

-          TG 0.8 mmol/L < 1.7: normal

-          Calculated LDL = 7.0 - 2.7 - (0.8/5) = 4.14 mmol/L > 4.1: increased risk

-          Limit of systolic blood pressure 133 mmHg

-          Risk factor: 3.4% compared with 2.6 % of normal people or 1.3 folds higher than average risk for  CVD than other cases same gender and age.

Case 3: 20 years old woman

-          Total cholesterol 3.6 mmol/L < 5.2: normal, optimal.

-          HDL-cholesterol 1.5 mmol/L > 1.0: a average high value

-          TG 0.8 mmol/L < 1.7: normal

-          Calculated LDL = 3.6 - 1.5 - (0.8/5) = 1.94 mmol/L < 2.6: optimal

-          Limit of systolic blood pressure 106 mmHg

-          Risk factor: 0.1% compared with 0.1% of normal people or no higher average risk for CVD than other cases same gender and age.

Case 4: 60 years old man

-          Total cholesterol 7.8 mmol/L > 6.2: level has more than twice the risk of coronary heart disease.

-          HDL-cholesterol 0.9 mmol/L < 1.0: low HDL- cholesterol. An increased risk factor for heart disease.

-          TG 2.5 mmol/L > 2.2: substantially increased risk

-          Calculated LDL = 7.8 - 0.9 - (2.5/5) = 6.4 mmol/L > 4.9: very high, substantially increased risk.

-          Limit of systolic blood pressure 125 mmHg

-          Risk factor: 57.7 % compared with 6.5 % of normal people or 9 folds higher risk for CVD than other cases of same gender and age on next 10 years.

References

1.      L. Kathleen Mahan, Sylvia Escott-Stump. Krause’s food and nutrition therapy. Edition 12, 2008.

2.       American Heart Association Nutrition Committee, Lichtenstein AH et al: Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006 Jul 4;114(1):82-96. Epub 2006 Jun 19.

3.       Hegsted DM, Ausman LM, Johnson JA, Dallal GE: Dietary fat and serum lipids: an evaluation of the experimental data. Am J Clin Nutr 57:875–883, 1993

4.      Mattson FH, Grundy, SM: Comparison of effects of dietary saturated, monounsaturated, and polyunsaturated fatty acids on plasma lipids and lipoproteins in man. J Lipid Res 26:194–202, 1985.

5.      Basu A et al. Dietary factors that promote or retard inflammation. Arterioscler Thromb Vacs Biol 26:995, 2006.

6.      Sacks FM et al. Soy protein, isoflavones, and cardiovascular health: a summary of a statement for professionals from the American Heart Association Nutrition committee. Arterioscler Thromb Vacs Biol 26:1689, 2006.

7.      Lichtenstein AH et al. Stanol/sterol ester-containing foods and blood cholesterol levels. Circulation 114: 82, 2006.

8.      Stefán E. Matthíasson. Kólesteról og blóðfitur. Fræðsluefni nota fyrir sjúklinga .Janúar, 2010.

9.      The Third Report of the Expert panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III or ATP III). May, 2001.

Iron dificiency anemia status of individuals

 What is iron dificiency

Iron deficiency is the most widespread nutrition disorder in the world and the primary cause of anemia (WHO, 2001). Iron deficiency anemia is rare in industrialized countries but is of high prevalence in developing countries (WHO & FAO 2004). Iron deficiency and iron deficiency anemia are defined as follows (Zimmermann 2005):

-           Iron deficiency is a reduction of iron in the body to the extent that cellular storage iron required for normal metabolic and physiological functions is fully exhausted, with or without anemia.

-           Iron deficiency anemia is defined as iron deficiency and low haemoglobin levels

1.      Indicators and measurements of iron status to evaluate iron dificiency anemia

The five main indicators of iron status (Transferrin, zinc protoporphyrin, haemoglobin, mean corpuscular volume and serum ferritin) outlined by WHO. Concentrations of serum ferritin, haemoglobin and mean corpuscular volume values were used to detect iron deficiency anemia and serum ferritin alone was used to screen for iron deficiency (Hallberg et al. 1993).

Haemoglobin (Hb)

Haemoglobin is the most widely used measure to assess iron status. Because hemoglobin levels drop relatively late in the development of iron deficiency it is usually used as a first factor to detect iron deficiency anemia but it has some limitations if used alone because of low specificity and sensitivity (Cook JD 2005). A lower than normal hemoglobin level indicates anemia. Haemoglobin is frequently used in conjunction with other variables such as mean corpuscular volume, red cell distribution and zinc protoporphyrin, to detect iron deficiency anemia. The cut-off points for haemoglobin (Hb (g/L)) proposed by WHO.                                                

Hb (g/L)

 Children 6 to 59 months          110

 Children 5-11 years                 115

 Children 12-14 years               120

 Non-pregnant women (≥ 15 y) 120

       Pregnant women                     110

       Men (≥ 15 y)                           130

Serum ferritin (SF)

Serum ferritin is considered to be the best single laboratory measure to detect iron status and iron deficiency (Borch-Ionsen 1995). This protein helps store iron in body, and a low level of ferritin usually indicates a low level of stored iron. The cut-off points for serum ferritin (SF (μg/L)) to detect iron deficiency anemia proposed by WHO criteria for the age groups.

                                    SF of male (μg/L)         SF of female (μg/L)

  < 5 years          < 12                             < 15

              ≥ 5 years          <15                              < 15

Table. Clinical findings

	Iron excess		Normal	Iron deficiency
	Stage 2 Iron overload	Stage 1 Positive iron balance	Normal	Stage 1 Early negative iron balance	Stage 2 Iron depletion	Stage 3 Damaged metabolism: iron deficient erythropoiesis	Stage 4 Clinical damage: iron deficiency anemia
Serum ferritin (μg/L)	> 300	> 150	100 ± 60	< 25	20	10	< 10

Krause’s Food and Nutrition Therapy p: 814-815.

     Mean corpuscular Volume

Mean corpuscular volume is a reliable but a relatively late indicator of nutritional iron deficiency that is widely used (Cook 2005). The cut-off points for mean corpuscular volume (MCV (fl)) to detect iron deficiency anemia, used in the NHANES II (Expert scientific working group, 1985).

MCV (fl)

Children 1-2 years                                     73 fl

Children 3-4 years                                     75 fl

Children 5-10 years                                   76 fl

Children and adolescents 11-14 years      78 fl

Adolescents and adults 15-74 years         80 fl

2.      Nutrients which could cause decrease of haemoglobin

Deficiency of nutrients intake such as meat, poultry and fish could cause reduction of haemoglobin. This is due to the primary source of heme iron is derived from hemoglobin and myoglobin found in meat, poultry, fish and seafood. The primary source of heme iron is derived from hemoglobin and myoglobin found in meat, poultry and fish. Non-heme iron is mainly found in plant-based foods such as cereals, pulses, fruits and vegetables [9].

Factors known to enhance absorption of non-heme iron are ascorbic acid (Vitamin C), the meat factor (meat, poultry, fish and other seafood) and alcohol. Factors known to inhibit iron absorption are phytate or inositol hexaphosphate (mostly found in bran products, seeds, cereals, legumes, fruits and vegetables), certain polyphenols (mostly found in tea, coffee, red wines, cocoa, spices, fruits and vegetables), calcium, eggs and soy proteins [4].

3.      Groups of people may be at higher risk of iron deficiency anemia [10]

Women

Because women lose blood during menstruation, women in general are at greater risk of iron deficiency anemia.

Infants and children

Infants, especially those who were low birth weight or born prematurely, who don't get enough iron from breast milk or formula may be at risk of iron deficiency. Children need extra iron during growth spurts, because iron is important for muscle development. If your child isn't eating a healthy, varied diet, he or she may be at risk of anemia.

Vegetarians

Because vegetarians don't eat meat, they're at greater risk of iron deficiency anemia. Iron that comes from grains and vegetables isn't absorbed by the body as well as is iron that comes from meat.

4.      Iron status of individuals

Individual 1 is a 60 years old man was diagnosed positive iron balance with Hb 140 g/L > 130 (normal), MCV 88 fl > 80 (normal) and SF 200 μg/L > 150 (high, see table 1).

Individual 2 is a 67 years old woman was diagnosed normal iron status with Hb 135 g/L > 120 (normal), MCV 86 fl > 80 (normal) and SF 150 μg/L (normal, see table 1).

Individual 3 is a 20 years old woman was diagnosed in status of iron deficiency anemia and iron deficiency in stage 4 with Hb 120 g/L (the cut-off points for haemoglobin to defect iron deficiency anemia), MCV 77 fl < 80 (low) and SF 9 μg/L < 10 (very low, iron deficiency stage 4, iron deficiency anemia and clinical damage).

Individual 4 is a 60 years old man was diagnosed iron overload status with Hb 150 g/L > 130 (normal), MCV 95 fl > 80 (normal) and SF 420 μg/L > 300 (very high, see table 1).

References

1.      WHO & FAO (2004): Vitamin and mineral requirements in human nutrition. 2nd ed. Iron: 246-278. Geneva: WHO.

2.      WHO (2001): Iron deficiency anaemia. Assessment, prevention and control. A guide for programme managers. WHO/NHD/01.3, Geneva: WHO.

3.      Zimmermann MB, Chaouki N & Hurrell RF (2005): Iron deficiency due to consumption of a habitual diet low in bioavailable iron: a longitudinal cohort study in Moroccan children. Am. J. Clin. Nutr. 81, 115-121.

4.      Hallberg L, Bengtsson C, Lapidus L, Lundberg P-A & Hulthén L (1993): Screening for iron deficiency: an analysis based on bone marrow examination and serum ferritin determinations in a population sample of women. Brit. J. Haematol. 85, 787-98.

5.      Cook JD (2005): Diagnosis and management of iron-deficiency anemia. Best Pract. Res. Clin. Haematol. 18, 319-322.

6.      Borch-Ionsen B (1995): Determination of iron status: brief review of physiologic effects on iron measures. Analyst 230, 891-893.

7.      Expert Scientific Working Group. (1985) Summary of a report on assessment of the iron nutritional status of the United States population. Am. J. Clin. Nutr. 42: 1318−1330.

8.      L. Kathleen Mahan, Sylvia ES. Krause’s Food and Nutrition Therapy. Edition 12, 2008.

9.      Hallberg L, Hulthen L & Gramatkovski E (1997): Iron absorption from the whole diet in men: how effective is the regulation of iron absorption? Am J. Nutr. 66, 347-56.

10. http://www.mayoclinic.com/health/iron-deficiency-anemia/DS00323/DSECTION=risk-factors