Definition: Lipids are compounds that are soluble in organic (non-polar) solvents but not in water—important because the human body is mostly water.
Table 5-1 “Usefulness of Fats” (high-level points)
• Energy source (concentrated kcal)
• Energy storage (adipose tissue)
• Padding & insulation of organs
• Cell membrane structure (phospholipid bilayer)
• Raw material for compounds such as hormones, bile, vitamin D
Dietary Recommendations for Fat
General (Table 5-2)
• Emphasize unsaturated fats; limit saturated & trans fats.
Polyunsaturated Fatty Acids (PUFA)
• Linoleic acid ((\omega 6)): 5\text{–}10\% of total kcal.
• Linolenic acid ((\omega 3)): 0.6\text{–}1.2\% of total kcal.
Cholesterol
• DRI: “Minimize” within a healthy diet rather than meet a fixed ceiling.
• Only about \frac13 of the population shows a marked blood-cholesterol drop when intake is lowered.
• Nutritious, cholesterol-rich foods—eggs, shellfish, liver—should be limited but not banned.
Classification of Lipids
Triglycerides
• \approx95\% of dietary & body fat.
• Structure: Glycerol backbone + 3 fatty acids (FA) (Fig 5-3).
• Glycerol can be synthesized from glucose or amino acids.
Fatty-acid chain length
• Short < 10 C; Medium 12\text{–}14 C; Long > 16 C.
• Shorter chains → softer, melt more readily.
Degree of saturation (Fig 5-5)
• Saturated (no C=C), solid at room T (butterfat, coconut oil, palm oil).
• Monounsaturated (1 C=C) – e.g., canola & olive oils.
• Polyunsaturated (≥2 C=C) – liquid oils from plants & fish.
Processing Effects & Trans Fats
Hydrogenation (margarine manufacture, Fig 5-12)
• Adds H to C=C, yielding “hard” fats that store better, resist rancidity, tolerate high frying temps.
• Produces trans-fatty acids → behave biologically like saturated FA; raise CVD risk.
Regulatory status
• Labels must list trans fats separately.
• 2018: Health Canada banned partially hydrogenated oils.
Phospholipids
• Structure: Glycerol + 2 FA + phosphate compound.
• Dual solubility (water & fat) → natural emulsifiers (lecithin in egg yolk).
• No special therapeutic properties claimed.
Sterols
• Cholesterol in cell membranes & bile; precursor for vitamin D, sex hormones (estrogen, testosterone) & stress hormones (epinephrine).
Digestion, Absorption & Transport
Stomach: fat separates from watery chyme; minimal digestion.
Small intestine (Fig 5-6)
• Bile from liver/GB emulsifies fat droplets.
• Pancreatic lipase splits TG → monoglycerides + FA + glycerol.
Absorption (Fig 5-9)
• Small lipids (short/medium FA & glycerol) enter portal blood directly.
• Large lipids (long FA & monoglycerides) are packed into chylomicrons → lymph → bloodstream.
Lipoproteins
• Chylomicron – transports dietary lipids.
• VLDL – exports TG made in liver to cells.
• LDL – delivers cholesterol to tissues (“bad”).
• HDL – scavenges cholesterol back to liver for excretion (“good”).
Metabolism & Energy Use
At rest, liver & muscle burn a mix ≈ 50\% carbohydrate / 50\% lipid.
For FA oxidation, carbohydrate must be available; if not, incomplete breakdown → ketones accumulate in blood & urine.
Blood Cholesterol & CVD Risk
High LDL raises heart-disease risk; low HDL also harmful.
Key modifiable risk pattern: diet high in saturated & trans fats + low produce & whole-grains.
Public media often simplifies or contradicts research.
Historic advice: cut total fat → unintended rise in refined carbs & sugars → diabetes/CVD.
Seven Countries Study
• Sat-fat intake closely tracks CHD deaths; total fat less predictive.
• Finland & Crete both high-fat; Finland had highest CHD deaths, Crete lowest (diet: mostly olive oil, sat-fat < 10\% kcal).
Current consensus
• Replace saturated fats with unsaturated (especially PUFA) & avoid trans fats.
• Health Canada claim: swapping sat-fat for MUFA/PUFA lowers cholesterol.
Ongoing questions
• Exact biological mechanisms; genetic variability; role of specific FA types.
• Some sat-FAs may be neutral; excess of certain PUFAs may be harmful.
Controversial meta-analysis found no sat-fat–CVD link → criticized for design flaws.