CHPLN cheat sheet

Holistic nutrition frames health as the interaction of biochemical, environmental, lifestyle, and psychosocial factors; assessment therefore spans diet, stress, sleep, movement, and environment rather than diet alone.

The six classes of nutrients are water, carbohydrates, proteins, fats, vitamins, and minerals; water is the only class required in gram-scale quantities daily and is often excluded from macronutrient counts.

Energy density: 9 kcal/g for fat, 7 kcal/g for alcohol, 4 kcal/g for carbohydrate and protein; alcohol is not a nutrient but contributes energy and displaces nutrient-dense intake.

The Dietary Reference Intakes comprise EAR (Estimated Average Requirement), RDA (Recommended Dietary Allowance = EAR + 2 SD), AI (Adequate Intake, used when an EAR cannot be set), UL (Tolerable Upper Intake Level), and AMDR (Acceptable Macronutrient Distribution Range).

AMDRs for adults: carbohydrate 45–65% of energy, fat 20–35%, protein 10–35%; protein RDA is 0.8 g/kg/day for healthy adults, higher in pregnancy, lactation, older adults, and catabolic states.

Nutrient density is nutrients per unit energy; energy density is energy per unit weight. Whole foods generally raise nutrient density and lower energy density relative to ultra-processed foods.

The holism principle holds that the whole diet pattern predicts outcomes better than isolated nutrients; single-nutrient supplementation trials often fail to replicate benefits seen with whole-food patterns.

Bioindividuality means genotype, microbiome, medications, life stage, and culture modify response to the same diet; two clients with identical intake can differ in absorption and metabolism.

Evidence hierarchy: systematic reviews and RCTs outrank observational cohorts, which outrank case reports and mechanistic speculation; mechanistic plausibility alone is insufficient to recommend an intervention.

Carbohydrate digestion: salivary and pancreatic alpha-amylase cleave starch to maltose and limit dextrins; brush-border maltase, sucrase, and lactase finish hydrolysis to monosaccharides absorbed via SGLT1 (glucose, galactose) and GLUT5 (fructose).

Protein digestion: gastric pepsinogen activated by HCl; pancreatic trypsin, chymotrypsin, and carboxypeptidases in the duodenum; brush-border peptidases and PepT1 absorb di- and tripeptides; amino acids enter via specific transporters.

Fat digestion: lingual and gastric lipase initiate hydrolysis; bile salts emulsify; pancreatic lipase with colipase generates 2-monoacylglycerol and free fatty acids; micelles deliver lipids to enterocytes, where chylomicrons form and enter lymph via lacteals.

Fatty acid classes: saturated (no double bonds), monounsaturated (one), polyunsaturated (two or more); omega-3 and omega-6 are essential PUFAs; alpha-linolenic acid (18:3 n-3) and linoleic acid (18:2 n-6) cannot be synthesized and require dietary intake.

Fiber: soluble/viscous fibers (beta-glucan, pectin, psyllium) slow gastric emptying and blunt postprandial glucose; insoluble fibers (cellulose, lignin) add bulk and speed transit; fermentable fibers yield short-chain fatty acids in the colon.

Fat-soluble vitamins (A, D, E, K) require bile and micellar solubilization and are stored in liver or adipose; water-soluble vitamins (B complex, C) are excreted more readily and have lower toxicity risk except B6 and niacin.

Key mineral interactions: calcium absorption is vitamin D–dependent and inhibited by phytate and oxalate; non-heme iron absorption is enhanced by vitamin C and inhibited by phytate, tannins, and calcium; zinc competes with iron and copper for absorption.

Vitamin D status is assessed by serum 25-hydroxyvitamin D; the active hormone is 1,25-dihydroxyvitamin D, produced in kidney and tightly regulated by PTH, calcium, and phosphate.

Iodine is required for thyroid hormone synthesis; selenium is a cofactor for deiodinases converting T4 to T3; both deficiencies can impair thyroid function independently of caloric intake.

Gut barrier: a single epithelial layer joined by tight junctions, covered by mucus, with secretory IgA and antimicrobial peptides; increased intestinal permeability is associated with inflammation but is not a stand-alone diagnosis.

Microbiome composition is shaped by delivery mode, breastfeeding, diet, antibiotics, geography, and age; diversity and stability are generally favorable markers, while dysbiosis describes compositional or functional imbalance.

Fermentable fibers and resistant starch are converted by colonic bacteria to short-chain fatty acids (acetate, propionate, butyrate); butyrate is the primary fuel for colonocytes and supports barrier integrity.

The low-FODMAP protocol restricts fermentable oligosaccharides, disaccharides, monosaccharides, and polyols for 2–6 weeks, followed by structured reintroduction; it is a symptom-management tool for IBS, not a long-term default diet.

Small intestinal bacterial overgrowth (SIBO) is diagnosed by breath testing or small-bowel aspirate culture; breath tests have variable sensitivity and specificity and results must be interpreted with symptoms.

Celiac disease is an autoimmune enteropathy triggered by gluten; serology (tTG-IgA with total IgA) plus duodenal biopsy is standard, and testing requires ongoing gluten intake to avoid false negatives.

Non-celiac gluten sensitivity is a diagnosis of exclusion after celiac disease and wheat allergy are ruled out; symptom response to blinded gluten challenge is the most reliable evidence.

Probiotic effects are strain-specific and dose-dependent; evidence is strongest for specific strains in antibiotic-associated diarrhea, infectious diarrhea, and some IBS subtypes; general immune claims are not established.

Gastroesophageal reflux management includes meal timing, portion size, weight management, and trigger identification; proton pump inhibitors reduce acid but do not address mechanical or lifestyle contributors.

Glycemic markers: fasting glucose, 2-hour oral glucose tolerance test, and HbA1c (reflects ~2–3 months of average glycemia); HbA1c can be misleading in anemia, hemoglobinopathies, pregnancy, and renal disease.

Insulin resistance precedes type 2 diabetes; surrogate markers include fasting insulin, HOMA-IR (fasting glucose × fasting insulin / 405), and triglyceride-to-HDL ratio.

Metabolic syndrome requires at least three of: elevated waist circumference, elevated triglycerides, low HDL, elevated blood pressure, elevated fasting glucose; thresholds are population-specific.

Thyroid: TSH is the first-line screen; free T4 and total/free T3 clarify status; Hashimoto's thyroiditis is identified by anti-thyroid peroxidase antibodies; thyroid hormone replacement dosing is influenced by absorption and binding.

Adrenal steroidogenesis follows the HPA axis: CRH → ACTH → cortisol; cortisol is highest in early morning and lowest around midnight; late-night salivary cortisol is used in suspected Cushing's syndrome.

PCOS diagnosis (Rotterdam criteria) requires two of: oligo/anovulation, clinical or biochemical hyperandrogenism, and polycystic ovarian morphology; insulin resistance is common and lifestyle intervention is first-line.

Type 2 diabetes remission is defined by HbA1c < 6.5% for at least 3 months without glucose-lowering medication; weight loss and energy restriction are the strongest levers.

Lipid targets are risk-based: LDL cholesterol is the primary target; statin benefit depends on absolute cardiovascular risk; dietary saturated fat raises LDL in most individuals, while replacing it with unsaturated fat lowers LDL.

Continuous glucose monitoring captures postprandial excursions that HbA1c misses; interpretation requires attention to sensor lag, compression artifacts, and individual glycemic variability.

The nutrition-focused physical exam screens for muscle wasting (temporalis, thenar, interosseous), subcutaneous fat loss, edema, and micronutrient signs such as glossitis, cheilosis, and koilonychia.

ABCDE assessment: Anthropometric, Biochemical, Clinical, Dietary, and Environmental/economic data; no single domain is sufficient for a diagnosis.

24-hour recall is quick but relies on memory and is subject to underreporting; food frequency questionnaires capture habitual intake but have limited precision; weighed food records reduce recall bias but increase burden.

Serum albumin and prealbumin are negative acute-phase reactants and reflect inflammation and hydration more than recent intake; they are not reliable markers of nutritional status in acute illness.

Iron studies: ferritin is the best single indicator of iron stores but rises with inflammation; transferrin saturation and soluble transferrin receptor help distinguish iron deficiency from anemia of inflammation.

Vitamin B12 assessment: serum B12 has limited sensitivity; methylmalonic acid and homocysteine rise in functional deficiency; intrinsic factor antibodies and parietal cell antibodies support pernicious anemia diagnosis.

Fat-soluble vitamin testing: serum retinol reflects vitamin A status only when stores are depleted; 25-hydroxyvitamin D is the standard vitamin D marker; vitamin K status is assessed by PIVKA-II or INR in specific contexts.

Reference intervals are population-based and do not define optimal function; results must be interpreted against symptoms, diet, medications, and clinical context.

Genetic testing (e.g., MTHFR variants) rarely changes clinical management on its own; genotype does not equal phenotype and should not replace functional or biochemical assessment.

Elimination diets follow a structured sequence: identify suspected triggers, eliminate for a defined period (often 2–6 weeks), reassess symptoms, reintroduce one food at a time, and document reactions.

The Mediterranean pattern emphasizes vegetables, legumes, whole grains, olive oil, fish, and moderate dairy, with limited red meat and processed foods; it has the strongest evidence base for cardiovascular and metabolic outcomes.

The DASH pattern targets blood pressure through potassium, calcium, magnesium, and fiber while limiting sodium; it is a dietary pattern, not a supplement protocol.

Ketogenic diets restrict carbohydrate to induce nutritional ketosis; monitoring includes electrolytes, renal function, lipids, and medication adjustment (especially insulin and sulfonylureas).

Low-carbohydrate and very-low-carbohydrate approaches improve short-term glycemic control in type 2 diabetes; long-term adherence and lipid response vary by individual.

Therapeutic diets must be matched to the client's culture, budget, cooking capacity, and medical history; an unfollowed ideal diet is inferior to a followed adequate one.

Food sensitivity testing (IgG panels, hair analysis, electrodermal testing) lacks validated diagnostic utility and is not a basis for elimination diets.

Personalization levers include genotype (limited utility), microbiome (emerging), medications, allergies, life stage, and preference; the strongest evidence supports phenotype- and preference-driven personalization.

Refeeding syndrome risk is highest with severe malnutrition, low BMI, minimal intake for more than 5 days, and electrolyte depletion; start low, go slow, and monitor phosphate, potassium, and magnesium.

Supplement regulation varies by country; in the United States, products are regulated as foods, not drugs, so efficacy and purity are not pre-market verified by the FDA.

Third-party testing (USP, NSF, Informed Sport) reduces but does not eliminate risk of contamination, adulteration, or mislabeling.

Herb–drug interaction mechanisms include CYP450 enzyme induction or inhibition, P-glycoprotein transport, and pharmacodynamic additivity; St. John's wort induces CYP3A4 and reduces efficacy of many drugs.

Common interaction examples: warfarin with ginkgo, garlic, or vitamin K–rich supplements; SSRIs with St. John's wort or 5-HTP (serotonin syndrome risk); thyroid medication with calcium or iron (absorption interference).

Dosing principles: start low, titrate slowly, document brand, dose, and duration; discontinue and reassess if new symptoms appear; check for pregnancy, lactation, and pediatric contraindications.

Adaptogens (e.g., ashwagandha, rhodiola) are claimed to modulate stress response; evidence is modest and product quality varies; thyroid and autoimmune conditions warrant caution with ashwagandha.

Omega-3 supplementation lowers triglycerides at higher doses; evidence for cardiovascular event reduction is mixed and depends on formulation, dose, and background diet.

Probiotic selection should specify genus, species, and strain, plus CFU count at end of shelf life; strain-specific evidence should match the clinical indication.

Micronutrient supplementation is indicated for documented deficiency, increased requirements, or restricted diets; megadose supplementation without deficiency carries risk and limited benefit.

The transtheoretical model stages are precontemplation, contemplation, preparation, action, maintenance, and termination; interventions should match stage rather than assume readiness.

Motivational interviewing uses open questions, affirmations, reflections, and summaries (OARS) to elicit change talk; the righting reflex (arguing for change) increases resistance.

Self-determination theory identifies autonomy, competence, and relatedness as basic psychological needs; supports that satisfy these needs improve intrinsic motivation and adherence.

SMART goals are specific, measurable, achievable, relevant, and time-bound; behavioral goals outperform outcome-only goals in the short term.

Sleep duration and quality affect appetite hormones (ghrelin, leptin), insulin sensitivity, and food choices; sleep assessment belongs in every nutrition intake.

Chronic stress elevates cortisol, which can increase visceral adiposity and appetite for energy-dense foods; mind-body practices (breathing, meditation, yoga) have modest but measurable effects on stress markers.

Physical activity guidelines for adults: at least 150 minutes of moderate-intensity aerobic activity or 75 minutes of vigorous activity weekly, plus muscle-strengthening on two or more days.

Coaching scope: behavior change support, education, and accountability; diagnosis, prescribing, and psychotherapy belong to licensed professionals.

Relapse is a normal part of behavior change; coaching should normalize it, identify triggers, and adjust the plan rather than treat it as failure.

Scope of practice is defined by law, credential, and training; nutrition professionals must not diagnose disease, prescribe medication, or provide psychotherapy unless separately licensed.

Informed consent covers purpose, methods, risks, benefits, alternatives, confidentiality limits, and the right to withdraw; it should be documented.

Confidentiality is limited by legal reporting requirements (e.g., suspected abuse, imminent harm) and by court order; clients should be told these limits at intake.

Referral triggers include red-flag symptoms (unintentional weight loss, dysphagia, blood in stool, new severe pain), abnormal laboratory values, eating disorder signs, and medication interactions.

Documentation should be objective, timely, and sufficient for another practitioner to understand the plan; subjective labels and speculation should be avoided.

Cultural humility requires recognizing the practitioner's own biases and adapting recommendations to the client's culture, language, and health literacy.

Conflicts of interest (supplement sales, affiliate relationships) must be disclosed; recommendations should be based on evidence, not revenue.

Professional boundaries include avoiding dual relationships, managing social media contact, and declining gifts or barter that could compromise objectivity.

Continuing education and staying current with evidence are ethical obligations; outdated practices should be revised when evidence changes.