functional med november Flashcards
1
Q
- What types of biochemical perturbations/lesions are predisposing and propagating factors involved in the etiology of chronic diseases?
A
a. Amino acid substitutions or deletions in protein primary structures - changes in higher order protein structures that affect structure and function - change cell architecture or enzyme activities. B. Toxicant may cause alterations in cell structural components or they may bind to enzyme active sites, blocking required biochemical pathways.
2
Q
- How does early detection of nutrient deficiency prevent chronic degenerative disease?
A
a. Early detection can lead to interventions that restore nutrient levels to values that enhance the recovery of normal cellular and tissue function.
3
Q
- How do standard therapeutic interventions for heart disease or depression affect a patient’s nutritional status?
A
a. Use of drugs like statins for atherosclerotic heart disease or SSRIs for depression serve to avert the short term effects of the disease, but they can exacerbate underlying nutrient insufficiencies or toxic effects.
4
Q
- As of 2001 (the year of publication for reference 317 of Chapter 4), how many genetic mutations of PAH were known to cause some variant of PKU?
In what enzyme? phenylalanine _________
A
a. 400, phenylalanine hydroxylase
5
Q
- What other enzyme is a principal cause of PKU?
hint _ _ _ cyclohydrolase
What is the biochemical relationship of this enzyme to the clearance of excess L-phenylalanine?
A
a. GTP cyclohydrolase
can have mutations that decrease the available levels of BH4 (Tetrahydrobiopterin)that is required as a coenzyme for Pulmonary hypertension (PAH)
6
Q
- For enzymes with vitamin-derived cofactor requirements, is there any difference between the clinical outcome from a genetic alteration in the protein structure and dietary deficiency of the nutrient required for production of the cofactor?
A
a. No.
Differences in manifestations arise the age of onset and severity of outcome from strongly disrupting genetic mutations.
7
Q
(CI 2.1) Why is it unusual to find elevated lipid peroxides when fat-soluble vitamins in serum are in their upper ranges? What does such a finding tell you about other nutrients that need evaluation?
A
• (CI 2.1) an indication that an individual has normal levels of protection against oxidative stress
- because many of the primary antioxidant functions are carried out by those vitamins, especially regarding biological membrane damage revealed by elevated lipid peroxides.
- The pattern found suggests that there may be elevated levels of membrane components that are easily oxidized, principally the polyunsaturated fatty acids.
8
Q
(CI 2.2) Which vitamin insufficiencies are indicated by elevated branched chain keto acids in urine?
B1, B2, B3, folate and lipoic acid
B1, B2, B3, B5 and lipoic acid
B1, B2, B3, B12 and lipoic acid
B1, B2, B3, B6 and lipoic acid
A
• (CI 2.2) Elevated BCKA indicates low activity for the BCKA dehydrogenase complex that can be caused by deficiencies for one of its 5 B-vitamin-derived coenzymes, B1, B2, B3, B5 and lipoic acid.
9
Q
(CI 2.3) How does urinary formiminoglutamate testing add clinical insight to homocysteine testing?
A
• (CI 2.3) Elevated HCys can be due to several factors, one of which is folate deficiency. Finding a normal level of FIGLU helps to rule that out as a cause.
10
Q
What organ failure most directly causes multiple low essential trace elements to be found in blood or urine? Why do such patients frequently show only slowly improving trace element status?
r
A
• (CI 3.1) Failure of hydrochloric acid output by the stomach reduced the digestion of dietary protein and the accompanying release of bound multivalent elements. Supplementing the elements without correcting the stomach acid deficiency may be poorly effective because (1) foods are the major source of daily element intake and (2) lack of properly timed pH shifts can interfere with the sequence of events required fodelivering added elemental salts to absorptive surfaces in the small intestine. Free amino acids and small peptides from dietary protein are often required intermediate ligands for element absorption.
11
Q
If you are called to review the records of a patient who has undergone multiple heavy metal detoxification procedures, what change in treatment is suspected when previously normal urinary mercury suddenly shows strong elevation?
A
• (CI 3.2) Rapid increase in Hg found in body fluids when no significant change in exposure has occurred could be due to either physician-guided chelation therapy or patient-administered forms of chelating agents such as sulfur amino acid that can mobilize Hg from deep sequestered sites such as bone.
12
Q
What amino acid evaluation would come to mind for a patient with chronic thyroid insufficiency?
A
• Low tyrosine and phenylalanine
13
Q
(pp 188-189) What effect does delayed specimen transport have on relative levels of glutamate (glu) and glutamine (gln)?
A
• (pp 188-189) Spontaneous hydrolysis of the amide side chain causes Gln conversion to Glu in specimens that are either delayed or warmed during transit.
14
Q
(pp 222-230) The reciprocal regulation of transmethylation and transulfuration of HCys shown in Fig. 4.20 translates to decreased availability of HCys for reformation of Met.
What pattern of amino acids in plasma might indicate chronic presence of such effects in a patient?
why would this happen?
A
The reciprocal regulation of transmethylation and transulfuration of HCys shown in Fig. 4.20 translates to decreased availability of HCys for reformation of Met as shown in Fig. 2.11. The reduced flow of Met tends to reduce available active methyl (S-adnosylmethionine) for all methylation reactions shown in Fig. 2.11. Multiple clinical outcomes can be associated with these competing demands for homocysteine.
15
Q
What body function uses the most amount of AA’s?
A
Protein synthesis is, by far, the greatest demand on absorbed amino acids, far outpacing other products such as neurotransmitters or hormones like thyroxin.
16
Q
A consequence of this fact (Protein synthesis is, by far, the greatest demand on absorbed amino acids) is that patients who show dramatic responses to therapies of customized essential amino acids are most likely demonstrating clinical effects of ____ ____ ____.
This is especially true regarding the organs with greatest turnover rates like the __1__ and 2. In the 2, the only process that can approach the magnitude of amino acid demand for protein synthesis is glutathione synthesis in a patient under chronic, severe oxidative or toxicant stress.
A
restored organ reserve
GI tract and liver
17
Q
(Fig 4.11) What compound is abbreviated “ADMA.” What cell regulator does elevated levels of ADMA in blood affect? What symptom is frequently produced?
A
ADMA stands for assymetric dimethylarginine
it inhibits nitric oxide synthase, regulating the multiple, powerful effects of that cell regulator.
Excessive ADMA frequently produces hypertension due to lack of NO to induce vasodilatation.
18
Q
(Fig 4.17) What elemental cofactor is required for conversion of dopamine to norepinephrine? For what enzyme?
And what vitamin derivative?
A
• (Fig 4.17) Copper ions are a critical cofactors required by dopamine hydroxylase.
also needs ascorbate
19
Q
why does finding a pattern of strongly elevated serine with low glycine on a plasma amino acid profile may be related to patient symptoms of poor growth, maldigestion, impaired cognition or excessive fatigue?
A
- Gly and Ser are related by a single reaction that transfers the hydroxymethyl group,
- they normally move up and down together on amino acid profiles.
- When they do not, then other pathway interferences are suspected, mainly glycine cleavage system
- genetic or toxicant interruption of that enzyme would tend to prevent the degradation of glycine.
- The resulting accumulation of glycine would tend to reduce activity of the Gly to Ser conversion, leading to such a pattern of elevated Gly and normal or low Ser.
-Since that pathway is a major source of single carbon for the THF pathways (Fig 2.11), multiple biosynthetic and methylation defect manifestations may be found.
20
Q
finding a pattern of strongly elevated serine with low glycine on a plasma amino acid profile, Which micronutrients are potential causes or confounding factors?
A
That system may be activated by added vitamin B6 or folate.
21
Q
finding a pattern of strongly elevated serine with low glycine on a plasma amino acid profile, : If your assessments indicate normal levels of those micronutrients (B6 or folate), what other explanation is likely for the amino acid abnormality pattern?
A
If various evaluations indicate normal levels of those vitamins, then a genetic polymorphism in the glycine cleavage system enzyme is indicated, as occurs in the condition known as non-ketotic hyperglycinemia.
22
Q
finding a pattern of strongly elevated serine with low glycine on a plasma amino acid profile: What further information about health effects related to the pattern is suggested by the information in Fig. 4.23?
A
• (Fig’s 4.22 and 4.23). Since that pathway is a major source of single carbon for the THF pathways (Fig 2.11), multiple biosynthetic and methylation defect manifestations may be found.
23
Q
Describe a typical procedure for producing a customized free-form amino acid product.
A
• (Fig 4.30b) performing a plasma amino acid profile and using the results to produce an essential amino acid mixture where the degrees of low levels in plasma govern amounts added for each amino acid. The usual dosing of the product for adults is a rounded teaspoon twice daily.
24
Q
(CI 4.3) What amino acid imbalance is indicative of ornithine transcarbamylase deficiency? Why?
A
• (CI 4.3) Genetic polymorphisms in any of the four enzymes of the urea cycle tend to produce strong elevations of urea cycle intermediate products measured in profiles of plasma amino acids. In the case of OTC deficiency, the greatest elevation is usually in its substrate, ornithine.
pg 201 -
25
Antidepressants can deplete
* B vitamins, Se, Zn, GSH, Ca, Mg, Vit C
* Low plasma AA
* AA’s, Cu, mercury toxicity, lithium def. low cholesterol, low GABA
* Mg, Tauu, Vitamin E
* B vitamins, low plasma AA
* Arg, Arsenic, beta carotene, Iodine, Niacin, Se, Strontium, Vitamin C, zinc
B vitamins, Se, Zn, GSH, Ca, Mg, Vit C
26
Diabetes can cause what Nutrient Def?
* B vitamins, Se, Zn, GSH, Ca, Mg, Vit C
* Low plasma AA
* AA’s, Cu, mercury toxicity, lithium def. low cholesterol, low GABA
* Mg, Tauu, Vitamin E
* B vitamins, low plasma AA
* Arg, Arsenic, beta carotene, Iodine, Niacin, Se, Strontium, Vitamin C, zinc
Mg, Tauu, Vitamin E
27
Heart disease can be related to what nutrient def.
* B vitamins, Se, Zn, GSH, Ca, Mg, Vit C
* Low plasma AA
* AA’s, Cu, mercury toxicity, lithium def. low cholesterol, low GABA
* Mg, Tauu, Vitamin E
* B vitamins, low plasma AA
* Arg, Arsenic, beta carotene, Iodine, Niacin, Se, Strontium, Vitamin C, zinc
* oxidative stress, nutrient def. insufficiency of antioxidants, toxicity. Arginine, niacin, CoQ10, vitamin C, E, B vitamins
(not listed in book)--oxidative stress, nutrient def. insufficiency of antioxidants, toxicity. Arginine, niacin, CoQ10, vitamin C, E, B vitamins
28
Cancer related nutrient def.
* B vitamins, Se, Zn, GSH, Ca, Mg, Vit C
* Low plasma AA
* AA’s, Cu, mercury toxicity, lithium def. low cholesterol, low GABA
* Mg, Tauu, Vitamin E
* B vitamins, low plasma AA
* Arg, Arsenic, beta carotene, Iodine, Niacin, Se, Strontium, Vitamin C, zinc
arginine, arsenic toxicity, beta carotene, iodine, niacin, selenium, strontium, vit C, zinc
29
Chronic fatigue related nutrient def.
* B vitamins, Se, Zn, GSH, Ca, Mg, Vit C
* Low plasma AA
* AA’s, Cu, mercury toxicity, lithium def. low cholesterol, low GABA
* Mg, Tauu, Vitamin E
* B vitamins, low plasma AA
* Arg, Arsenic, beta carotene, Iodine, Niacin, Se, Strontium, Vitamin C, zinc
Low plasma AA
30
Depression related nutrient def.
* B vitamins, Se, Zn, GSH, Ca, Mg, Vit C
* Low plasma AA
* AA’s, Cu, mercury toxicity, lithium def. low cholesterol, low GABA
* Mg, Tauu, Vitamin E
* B vitamins, low plasma AA
* Arg, Arsenic, beta carotene, Iodine, Niacin, Se, Strontium, Vitamin C, zinc
B vitamins, low plasma AA
31
Autism related nutrient def.
* B vitamins, Se, Zn, GSH, Ca, Mg, Vit C
* Low plasma AA
* AA’s, Cu, mercury toxicity, lithium def. low cholesterol, low GABA
* Mg, Tauu, Vitamin E
* B vitamins, low plasma AA
* Arg, Arsenic, beta carotene, Iodine, Niacin, Se, Strontium, Vitamin C, zinc
AA metabolism, copper, mercury toxicity, lithium def. low cholesterol, low GABA (gamma-aminobutyric acid)
32
Why does direct testing of calcium in body fluids fail to reveal nutritional status of calcium?
what is the proper method?
Measuring calcium in body fluids or tissues provides only the status of ionic calcium that is highly regulated and shows little variation over a wide range of balance conditions.
Bone mineral density (BMD) provides the best measurement of calcium status. Calcium is mainly stored in the bones.
33
(CI 4.7) Corrections of what four amino acid insufficiencies are found to be helpful in anxiety? Why?
* Ly, Gly, Trp, Phe
* Lys, Gly, Tau, Phe
* Ly, Gly, Tau, Proline
* Lys, Gly, Tyr, Phe
• (CI 4.7) Patients with anxiety related to imbalanced brain neurotransmitter function may respond to amino acids that act directly as receptor antagonists (Lys, Gly, Tau) or serve as precursors to neurotransmitters (Phe).
34
What patterns indicate customized, free-form amino acids?
• Various patterns where some EAA are low and others are normal or elevated suggest specific pathways are activated causing individual amino acid depletions. This pattern is most famously found as low L-Trp in patients on SSRI medications that increase the demand for serotonin formation from tryptophan.
35
What AA patterns indicate glutathione stress? (6 AAs)
What 2 kinds of stress causes this?
What do the patterns of lower levels and greater numbers of those amino acids are found indicate?
• Low levels of the amino acids that either directly or indirectly participate in GSH formation (Met, Tau, HCys, Gly, Ser, Thr) may be due to chronic oxidative or toxicant stresses that chronically increase demand for glutathione that the liver attempts to supply via higher rates of GSH synthesis.
Patterns of lower levels and greater numbers of those amino acids are found low emerge, give indications of more and more severe GSH stress that may require more aggressive interventions with amino acids and investigation of causes.
36
(pp 272-273) Into what categories are the fatty acids typically placed on laboratory reports?
chain length within each greater category or desaturation level or
PUFA omega double bond position.
37
(pp 287-288) What fatty acid is part of the structure of the most active endocannabinoids?
(pp 287-288) The endocannabinoids of greatest physiological activity are derived from arachidonic acid.
38
(pp 298-299) Which omega-3 fatty acid tends to become persistently low in patients using fish oil supplements?
potentially clinically low levels of AA.
• (pp 298-299) When fish oil supplements are used excessively, the superior binding of the n-3 fatty acids to desaturase enzymes tends to suppress the desaturation of linoleic and GLA to form AA, casing potentially clinically low levels of AA.
39
(Fig. 5.2) Composition of which lipoprotein is largely revealed in measurements of both serum triglycerides and plasma fatty acids?
largely LDL particles.
• (Fig. 5.2) Since specimen collection for both serum triglycerides and plasma fatty acids is done in the fasting state, the circulating form of lipoprotein is largely LDL particles.
40
(Table 5.2) Which foods are particularly rich in linoleic acid?
* evening primrose, safflower, grape seed, sunflower and hemp
* Fish oil, avocado, coconut oil
* flax, primrose, or black current oils
* Palm oil, butter, cheese and meats
```
cooking oils?
• coconut, cottonseed and peanut
• corn, cottonseed and olive
• corn, cottonseed and peanut
• olive, cottonseed and peanut
```
(order of potency) evening primrose, safflower, grape seed, sunflower and hemp.
with the notable exception of olive oil, LA is a major ingredient in all of the oils commonly used in cooking, including corn, cottonseed and peanut.
41
(Fig 5.9) There is a requirement to perform a 2-carbon removal from the carboxyl group end of the 24:6n3 intermediate that is not possible inside mitochondria. What cellular organelle other than mitochondria is required for VLCFA degradation? What clinical consequence is common in pregnancy?
•
peroxisomes
The VLCFA intermediate must be transported out of the mitochondria and into the peroxisomes in order to generate DHA that is critical for infant brain development. Thus, infants delivered by women who are deficient in DHA take a long time to develop their own DHA levels from dietary precursors.
42
18:1n9
```
Linoleic acid (LA)
Oleic Acid (OA)
α-linolenic (ALA)
```
Oleic Acid (OA)
43
18:2n6
```
Linoleic acid (LA)
Oleic Acid (OA)
α-linolenic (ALA)
```
Linoleic acid (LA)
44
20:4n6
```
eicosapentaenoic acid (EPA)
Arachidonic acid (AA)
Linoleic acid (LA)
```
Arachidonic acid (AA)
45
20.5n3
```
eicosapentaenoic acid (EPA)
Arachidonic acid (AA)
α-linolenic (ALA)
```
eicosapentaenoic acid (EPA)
46
(Fig 5.12) What essential nutrient other than PUFAs is required to stimulate peroxisome proliferation? How does this broaden clinical outcomes due to deficiency of that nutrient?
• Vitamin A as, 9-cis-retinoic acid
(Fig 5.12) Activation of the PPAR requires simultaneous binding of a PUFA and vitamin A as, 9-cis-retinoic acid.
Since peroxisome proliferation is a fundamental cellular response to energetic and immunological stressors, any condition that might require those systems may be impacted by deficiencies of PUFAs or vitamin A.
47
what is PPAR?
Peroxisome proliferator-activated receptors (PPARs)
are ligand-activated transcription factors of nuclear hormone receptor superfamily.
comprising of the following three subtypes: PPARα, PPARγ, and PPARβ/δ.
48
_____ function in the metabolism of fatty acids to help rid the cell of toxic peroxides and provide other essential metabolic functions.
peroxisomes
49
(Table 5.5) Would the symptoms associated with linoleic acid deficiency best be described as diverse or specific? Why?
• (Table 5.5) Highly diverse symptoms have been found in linoleic acid deficiency because of its central role in two processes that broadly impact cellular function. They are 1) cell membrane properties that affect membrane-bound protein complexes and receptors in all tissues and 2) formation of the dominant eicosanoid precursors, GLA and AA.
50
what intervention for: classic essential fatty acid deficiency
* corn or safflower oil
* fish oil, avoid hydrogenated oils
* good quality fats and oils
* n3 PUFAs, (use n PUFAs with caution)
good quality fats and oils
51
what intervention for: linoleic acid insufficiency
* corn or safflower oil
* fish oil, avoid hydrogenated oils
* good quality fats and oils
* n3 PUFAs, (use n PUFAs with caution)
corn or safflower oil
52
what intervention for: long chain PUFA dependent neuromembrane function.
* corn or safflower oil
* fish oil, avoid hydrogenated oils
* good quality fats and oils
* n3 PUFAs, (use n PUFAs with caution)
fish oil, avoid hydrogenated oils
53
what intervention for: low stearic to oleic ratio.
* corn or safflower oil
* fish oil, avoid hydrogenated oils
* good quality fats and oils
* n3 PUFAs, (use n PUFAs with caution)
n3 PUFAs, (use n PUFAs with caution)
54
what intervention for:low GLA and DGLA
* flax, primrose, or black current oils
* Primrose
* restrict booze, add lecithin, increase Met
* Vitamin e, and C, Se Mn, Zn
primrose
55
Fatty liver: what intervention for: saturated and Omega-9 (greek w-9) accumulation in the liver
pg 294
* flax, primrose, or black current oils
* Primrose
* restrict booze, add lecithin, increase Met
* Vitamin e, and C, Se Mn, Zn
restrict booze, add lecithin, increase Met
56
what intervention for:high PUFA intake without antioxidants
* flax, primrose, or black current oils
* Primrose
* restrict booze, add lecithin, increase Met
* Vitamin e, and C, Se Mn, Zn
Vitamin e, and C, Se Mn, Zn
57
what intervention for: Alpha or gamma linolenic acid insufficiency
* flax, primrose, or black current oils
* Primrose
* restrict booze, add lecithin, increase Met
* Vitamin e, and C, Se Mn, Zn
flax, primrose, or black current oils
58
(CI 5.1) Describe the fatty acid profile imbalance that tends to exaggerate inflammatory responses?
* Generally low levels of n-6 PUFAs, and especially EPA along with elevated AA.
* Generally low levels of n-3 PUFAs, and especially DHA along with elevated AA.
* Generally low levels of n-6 PUFAs, and especially EPA along with elevated ALA.
* Generally low levels of n-3 PUFAs, and especially EPA along with elevated AA.
generally low levels of n-3 PUFAs, and especially EPA along with elevated AA.
59
(CI 5.3) What essential fatty acid is likely to be found low in patients on aggressive, long-term omega-3 therapy?
* AA is elevated and EPA is low.
* DHA is elevated and AA is low.
* EPA is elevated and AA is low.
* EPA is elevated and ALA is low.
EPA is elevated and AA is low.
(CI 5.3) See response to pp. 298-99 question above. In that CI, EPA is elevated and AA is low.
• When fish oil supplements are used excessively, the superior binding of the n-3 fatty acids to desaturase enzymes tends to suppress the desaturation of linoleic and GLA to form AA, casing potentially clinically low levels of AA.
60
(CI 5.6) What clinical syndrome is indicated by finding a “greater than” sign in the family of saturated fatty acids?
•
(CI 5.6) Conditions variously known as “syndrome X”, “metabolic syndrome”, “prediabetes”, “hyperinsulinemia”, or “dysinsulinemia” tend to produce patterns seen as palmitic and stearic acids dominating the family of saturated fatty acids. This relationship is a confirmation of chronic stimulation of endogenous fatty acid synthesis by chronic episodes of elevated insulin.
61
```
what two fatty acids are known to dominate the family of saturated fatty acids in the presence of metabolic syndrome?
• lauric and stearic
• oleic and stearic
• palmitic and arachidic
• palmitic and stearic
```
palmitic and stearic acids dominating the family of saturated fatty acids.
62
(CI 5.7) Adrenoleukodystrophy is associated with what pattern of fatty acid abnormalities?
X-linked Adrenoleukodystrophy (ALD) is one of a group of genetic disorders called the leukodystrophies that cause damage to the myelin sheath, an insulating membrane that surrounds nerve cells in the brain.
• (CI 5.7) The etiology of adrenoleukodystrophy is lack of peroxisome activity required for oxidation and clearance of VLCFA. Those fatty acids accumulate massively, producing chronically progressive neuropathic symptoms in the patients.
On Sat FA table it looks like a diagonal line from top left to bottom right.
63
sources of palmitic FA
* evening primrose, safflower, grape seed, sunflower and hemp
* Fish oil, avocado, coconut oil
* flax, primrose, or black current oils
* Palm oil, butter, cheese and meats
Palm oil, butter, cheese and meats
64
(pp 327-329) Name the primary organic acid abnormalities that occur in carnitine deficiency.
• (pp 327-329) Elevated adipate, suberate and ethylmalonate
65
(pp 336-337) What patterns of abnormalities distinguish mitochondrial inefficiency from ammonia challenge as a cause of citric acid elevation? (4 markers)
• (pp 336-337) Ascribe high levels of citrate, aconitate and isocitrate to ammonia when (a) Only citrate, aconitate and isocitrate are found high or (b) orotate is concurrently elevated.
66
(pp 355-359) What does NMDA stand for?
These receptors are agonized by _____ acid and potentiated by ______ acid resulting in potential glutamate toxicity in neurons.
quinolinic, picolinic
picolinic, quinolinic
pyruvate, ethylmalonate
ethylmalonate, pyruvate
abbreviation for the N-methyl-D-aspartic acid class of ionotropic glutamatergic neuron receptors.
quinolinic, picolinic
67
pp 360-361) What urinary organic acid elevation may justify specifically aggressive vitamin C supplementation?
8-OHdG
p-hydroxyphenyllactic acid
2 0 methylhippurate
sulfate
• (pp 360-361) Aggressive vitamin C therapy may help to reduce elevated p-hydroxyphenyllactic acid and the concomitant elevated cell division rate stimulation that tends to produce systemic oxidative stress.
p-hydroxyphenyllactic acid
68
• (p 361) Failure of the reciprocal regulation can impair up-regulation of hepatic glutathione synthesis as the major response to oxidative stress, leading to exacerbated and prolonged cellular (esp. mitochondrial) damage from oxidant effects.
Is related to what OA metabolite
8-hydroxy-2'-deoxyguanosine (8-OHdG)
69
Why is supplementation with glucarate salts NOT indicated by abnormalities in urinary glucarate?
• (pp 364-365) Urinary glucarate is a marker of increased hepatic detoxification system activity. It is a by-product of pathways leading to glucuronic acid formation. Oral glucarate is not helpful for assisting hepatic detoxification or for relieving potential elevated rates of intestinal bacterial glucuronide hydrolysis.
70
(p 366) What is the implication of LOW homocysteine for the likelihood of finding elevated alpha-hydroxybutyrate?
• (p 366) Elevated AHB signals up-regulated hepatic glutathione synthesis, and that process demands flow of HCys into L-Cys formation to form gamma glutamyl-cystinyl-glycine (glutathione). Thus, low plasma HCys can signal a late-stage of chronic glutathione depletion where total body sulfur amino acid availability is failing to keep up with the demand.
71
low plasma HCys can signal a late-stage of chronic ________ depletion where total body sulfur amino acid availability is failing to keep up with the demand.
glutathione
72
(p 375) Explain how elevated benzoate can be a marker of either impaired detoxification or intestinal bacterial overgrowth. What other biomarker can help to differentiate the two scenarios?
• (p 375) Benzoate can become elevated due to
(a) failure of hepatic clearance by hippurate formation (impaired detoxification) or
(b) to elevated levels of benzoate release from dietary polyphenols by intestinal bacteria overgrowth where the hepatic clearance system capacity is exceeded.
If hippurate is normal or low, then scenario (a) is confirmed.
If hippurate is concurrently elevated, then scenario (b)
73
• (pp 387 - 388) _________ is a five carbon sugar found in grapes and other fruits and vegetables. It is a substrate for growth of some bacteria.
______ is the corresponding sugar alcohol that is formed by conversion of dietary carbohydrates by intestinal Candida species, and it serves as a biomarker of overgrowth, including severe, invasive candidiasis.
Arabinose, Arabinitol
74
(Table 6.3) Which organic acids become elevated in maple syrup urine disease?
• (Table 6.3) Genetic abnormalities in maple syrup urine disease generally reduce the activity of branched chain keto dehydrogenase, resulting in elevated levels of a-ketoisocaproate, a-ketoisovalerate, and a-keto-b-methylisovalerate.
75
Which organic acids are used to discriminate potential vitamin deficiencies causing homocysteine elevation?
• (Table 6.7) Homocysteine elevation can result from deficiencies of folate or vitamin B12 that are revealed by elevations of FIGLU and methylmalonate, respectively.
76
• (Figure 6.14 & 6.15) Vitamin B6 deficiency causes impairment of the hepatic kynurenine pathway that is used to convert tryptophan into nicotinic acid.
* B5, taurine
* B5, tryptophan
* B6, taurine
* B6, tryptophan
The pathway steps that are affected result in accumulation of ______ acid and, secondarily, kynurenic acid.
* Xanthurenic
* Arachidonic
* Behenic
* Nicotinic
B6, tryptophan
xanthurenic
77
Figure 6.2 draws attention to the selective permeability of the mitochondrial membranes that are regulated by transport proteins. Those actions allow specific citric acid cycle intermediates to easily leave so that their levels do not become _______.
elevated
(CI 6.3) An uninformed interpretation of the bold arrow that forms the central circular pattern in the figure might be that interruption at any single step would always cause low levels of the product for that step and high levels of the substrate and all preceding intermediates.
78
(CI 6.7) What facts in the patients’ history might explain the elevated glucarate finding?
• (CI 6.7) Cigarette smoking and therapeutic drugs cause increased activity in hepatic detoxification pathways, producing elevated glucarate.
79
CI 6.8) What does a 6-month progressive lowering of urinary sulfate with persistent elevation of pyroglutamate imply about a patients’ prognosis?
What specific nutrient interventions are indicated?
* Glucosamine
* Glutamate
* Glutamine
* Glutathione
in a state of chronic toxicant challenge or oxidative stress, and a concurrent, persistently elevated pyroglutamate indicates that renal losses of glutathione may be a contributing factor.
Glutathione support via preformed GSH or its precursor amino acids Cys, Met, Gly and related amino acids, Tau, Ser, Thr may be helpful for restoring GSH status.
80
What AAs are the precursors to glutathione? (3)
Cys, Met, Gly
81
What AAs may be helpful for restoring GSH status.
Tau, Ser, Thr
82
(pp 418-420) Give a metabolic rationale for the high incidence of hypochlorhydria.
What specific laboratory abnormalities are associated with insufficiency of stomach acid?
(pp 418-420) The generally recognized decline in stomach acid output with age is probably associated with underlying metabolic changes tied to nutrient insufficiencies and toxicant effects.
The gastric pit parietal cells are a focal point of those interactions due to their intense, post-prandial energetic (mitochondrial) demands during active HCl secretory episodes.
Insufficiencies of factors like zinc and biotin for support of protein synthesis and of B complex vitamins, iron and coenzyme Q10 for sustaining the multiple phases of mitochondrial activity can lead to impaired output of HCl.
That impairment leads to impaired digestion of dietary protein and poor release of major and trace elements from binding sites on food macromolecules.
83
What insufficiencies are linked to hypochlorhydria
* Vitamin C, E, B2, B3, Selenium
* Vitamin E, C, A, B2, B3
* Zinc, biotin, iron , coenzyme Q10
Zinc, biotin, iron , coenzyme Q10
84
(pp 420-422) Describe the patterns of abnormalities in stool chemistries found in conditions of (1) low stomach acid,
* stimulation of certain bacterial strains that metabolize amino acids.
* Constant infusion of excessive levels of periodontal bacteria such as Fusobacteria tends to shift the intestinal Microbiome into abnormal commensal population distributions.
* leaving normally absorbed dietary components (even carbs) in the intestinal lumen where microbe growth is stimulated due to the availability of growth substrate
Constant infusion of excessive levels of periodontal bacteria such as Fusobacteria tends to shift the intestinal Microbiome into abnormal commensal population distributions.
(pp 420-422) (1)Lack of stomach acid impairs the normal gastric suppression of microbes entering either from food or from populations resident in periodontal sites of the oral cavity. Constant infusion of excessive levels of periodontal bacteria such as Fusobacteria tends to shift the intestinal Microbiome into abnormal commensal population distributions.
85
(pp 420-422) Describe the patterns of abnormalities in stool chemistries found in conditions of, (2) low pancreatic enzymes
* stimulation of certain bacterial strains that metabolize amino acids.
* Constant infusion of excessive levels of periodontal bacteria such as Fusobacteria tends to shift the intestinal Microbiome into abnormal commensal population distributions.
* leaving normally absorbed dietary components (even carbs) in the intestinal lumen where microbe growth is stimulated due to the availability of growth substrate
(2) Insufficient pancreatic enzyme activities in the gut decreases digestion of dietary components (esp. protein), resulting in stimulation of certain bacterial strains that metabolize amino acids.
86
(pp 420-422) Describe the patterns of abnormalities in stool chemistries found in conditions of (3) impaired small bowel absorption.
* stimulation of certain bacterial strains that metabolize amino acids.
* Constant infusion of excessive levels of periodontal bacteria such as Fusobacteria tends to shift the intestinal Microbiome into abnormal commensal population distributions.
* leaving normally absorbed dietary components (even carbs) in the intestinal lumen where microbe growth is stimulated due to the availability of growth substrate
(3) leaving normally absorbed dietary components (even carbs) in the intestinal lumen where microbe growth is stimulated due to the availability of growth substrate
87
(pp 426 – 437) Compare and contrast the clinical values of lactulose-mannitol challenge testing and IgG4 testing.
• (pp 426 – 437) The introduction of a non-absorbed simple sugar (lactulose) along with one that normally is well absorbed (mannitol) directly into the GI tract provides a direct assessment of upper intestinal small molecule absorption.
It does not, however, answer the question of whether macromolecules from food are regularly penetrating the intestinal barriers and producing immunological consequences.
A positive answer to that question is directly provided by finding elevated levels of specific serum IgG4 anti-food component antibodies.
88
(pp 434-435) How does complement cascade activation explain differences between clinical interpretations of elevated serum IgG1 and IgG4-class antibodies to food antigens?
What is the final site for “digestion” of dietary proteins that are incompletely hydrolyzed by digestive enzymes?
• (pp 434-435) When food components first start to penetrate the intestinal barriers, they produce rapid production of the IgG1 class of antibodies. That class of antibodies bind with specific macromolecules from the food and are then recognized by Kupfer cell surface receptors in the hepatic arterioles, triggering the complement system to degrade the Ag-Ab complexes, completing the digestion of the food components.
Complement proteins, however, fail to recognize IgG4 food component complexes, allowing them to stay in systemic circulation for long periods (many days or weeks).
89
• (Figure 7.4) Lymphatic system lacteals of Fig. 7.4 carry dietary fats as _________ to the liver via entering the circulatory system at the left subclavian vein. As the post prandial blood flow enters the liver, the processing shown in Fig. 5.2 occurs.
* Chylomicrons
* HDL
* LDL
* VLDL
chylomicrons
90
(• (Table 7.5) The ammonuria indicated by elevated __1__ in CI 6.7 suggest that bacteria genera capable of high ___2___ production are abundant. (3 markers)
orotate
ammonia
Clostridia, Enterobacter and Bacillus spp.
91
(p 472) Below the threshold dose, how do responses predicted by the hormesis model differ from those derived from the threshold model? How does this theoretical framework help to explain observation such as?
- Lower incidence of breast cancer in women who smoke tobacco
- Apparent efficacies of homeopathic medicines
•
(p 472) While the threshold model presumes nil response below the threshold for positive responses, the hormesis model predicts (or allows) negative responses in the regions below the threshold for positive responses.
Thus, the hormesis model can explain how levels tobacco smoking below the threshold for increasing cancer incidence might produce lower risk via mechanisms such as induction of hepatic detoxification systems that lower total body estrogen exposure.
Similarly, the toxicities of many natural substances could produce positive effects at very low levels below which no toxicity can be seen.
92
(pp 77-78 & p 477) Why does oral DMSA cause dramatic increases in urinary elemental levels in patients with high body burdens of toxic elements?
think chelation
• (pp 77-78 & p 477) When a patient with a high body burden of a toxic element starts DMSA therapy, loses on a given day may be offset by release of the element from deep stores such as bone over a time interval longer than the urine collection during the therapy. The DMSA can act to stimulate mobilization of old pools with slow turnover.
93
(p 498) What compound reacts with acetaminophen to initiate mercaptan formation?
* Glutamine
* Glutathione
* Vitamin A
* Vitamin C
* Vitamin E
How does this explain the potential for uncontrolled oxidative stress and organ failure due to overdosing of drugs like acetaminophen?
• (p 498) Glutathione is the initial substrate required for mercaptan formation from acetaminophen.
This explains the potential for uncontrolled oxidative stress and organ failure due to overdosing of drugs like acetaminophen that produce high demand for hepatic glutathione conjugation.
94
• (Figure 8.4) Consider four individuals. The first has intestinal hyperpermeability (barrier weakness), the second has genetic defects in hepatic Phase II biotransformation enzymes, and the third has renal impairment that slows elimination, while the fourth has none of these issues. For the same exposure to organotoxicants, the first 3 may have diverse organ system clinical signs due to toxic effects while the fourth has no symptoms from the exposure. Why?
* genetic differences in barriers
* biotransofrmation,
* elimination
* all of the above
* none of the above
* a and c only
genetic differences in barriers, biotransofrmation, elimination
can also show up as different ailments
95
(Figure 8.5 and text) What micronutrient is specifically likely to assist the patient with elevated benzoate?
* Glycine, B5
* Glycine, THF
* Lysine, B5
* Lysine THF
• (The reaction requires formation of the benzoyl-Coenzyme A activate form, and very high rates of the pathway can produce losses of Coenzyme A that requires reformation from pantothenic acid.
So, in addition to supplementing GLYCINE, the patient may benefit from extra intake of PANTOTHENATE to maximize the rate of glycine conjugation and benzoate clearance.
Altough benzoic acid has low toxic potential, many other compounds that may not have been measured must flow through the same biotransformation pathway for clearance.
96
why does Elevated urinary benzoate arise?
Figure 8.5 and text) Elevated urinary benzoate arises when the hepatic Phase II glycine conjugation pathway fails to meet the demand for clearing benzoic acid.
97
_______ ____ is a fungistatic compound that is widely used as a food preservative
Benzoic acid is a fungistatic compound that is widely used as a food preservative
98
(Fig. 9.2) What essential trace elements are involved in protecting against oxidative stress?
* A and E
* A and D
* D and C
* E and C
• A and E
99
(Fig. 9.4) Note the central roles of glutathione in multiple mechanisms for responding to oxidative stress and the micronutrients needed to maintain cellular status of reduced and oxidized agents.
I removal of hydrogen peroxide:
* NADP+, NADPH,
* Vitamin C, E, B2, B3, Selenium, NADP+, NADPH, FAD
* Vitamin E, C, A, B2, B3, Selenium, NADP+, NADPH, FAD
• I removal of hydrogen peroxide: Vitamin E, C, A, B2, B3, Selenium, NADP+, NADPH, FAD
100
(Fig. 9.4) Note the central roles of glutathione in multiple mechanisms for responding to oxidative stress and the micronutrients needed to maintain cellular status of reduced and oxidized agents.
Membrane transfer:
* NADP+, NADPH,
* Vitamin C, E, B2, B3, Selenium, NADP+, NADPH, FAD
* Vitamin E, C, A, B2, B3, Selenium, NADP+, NADPH, FAD
• Membrane transfer: Vitamin C, E, B2, B3, Selenium, NADP+, NADPH, FAD
101
(Fig. 9.4) Note the central roles of glutathione in multiple mechanisms for responding to oxidative stress and the micronutrients needed to maintain cellular status of reduced and oxidized agents:
Lipoic acid for regeneration of oxidized form of glutathione and thioredoxin:
* NADP+, NADPH,
* Vitamin C, E, B2, B3, Selenium, NADP+, NADPH, FAD
* Vitamin E, C, A, B2, B3, Selenium, NADP+, NADPH, FAD
• Lipoic acid for regeneration of oxidized form of glutathione and thioredoxin: NADP+, NADPH,
102
(pp. 523-531) Note the array of biomarkers that can reveal the status of: Lipid oxidation
* 3-nitrotyrosine (3NT), Methionine sulfoxide
* DNA strand breakage (comet assay)
* Malondialdehyde (lipid peroxides), Isoprostanes, 4-hydroxy-2-Nonenal, Oxidized LDL
* P-Hydroxyphenyllactate, Homogentistate
* ROS production, Neutrophil mediated oxidative burst, antimicrobial mechanism, Increased oxidative stress associated with infection including H pylori, prevotella intermedia and Brucella melitensis
o Malondialdehyde (lipid peroxides)
o Isoprostanes
o 4-hydroxy-2-Nonenal
o Oxidized LDL
• TREATMENT: increase balanced antioxidant intake and decrease oxidant load. Use high dose individual antioxidants as indicated by laboratory testing.
103
(pp. 523-531) Note the array of biomarkers that can reveal the status of: Protein oxidation
* 3-nitrotyrosine (3NT), Methionine sulfoxide
* DNA strand breakage (comet assay)
* Malondialdehyde (lipid peroxides), Isoprostanes, 4-hydroxy-2-Nonenal, Oxidized LDL
* P-Hydroxyphenyllactate, Homogentistate
* ROS production, Neutrophil mediated oxidative burst, antimicrobial mechanism, Increased oxidative stress associated with infection including H pylori, prevotella intermedia and Brucella melitensis
o 3-nitrotyrosine (3NT)
o Methionine sulfoxide
• TREATMENT: increase balanced antioxidant intake and decrease oxidant load. Use high dose individual antioxidants as indicated by laboratory testing.
104
(pp. 523-531) Note the array of biomarkers that can reveal the status of: Nucleotide oxidation
* 3-nitrotyrosine (3NT), Methionine sulfoxide
* DNA strand breakage (comet assay)
* Malondialdehyde (lipid peroxides), Isoprostanes, 4-hydroxy-2-Nonenal, Oxidized LDL
* P-Hydroxyphenyllactate, Homogentistate
* ROS production, Neutrophil mediated oxidative burst, antimicrobial mechanism, Increased oxidative stress associated with infection including H pylori, prevotella intermedia and Brucella melitensis
o DNA strand breakage (comet assay)
• TREATMENT: increase balanced antioxidant intake and decrease oxidant load. Use high dose individual antioxidants as indicated by laboratory testing.
105
((pp. 523-531) Note the array of biomarkers that can reveal the status of: Endogenous Oxidative Stress modulators
* 3-nitrotyrosine (3NT), Methionine sulfoxide
* DNA strand breakage (comet assay)
* Malondialdehyde (lipid peroxides), Isoprostanes, 4-hydroxy-2-Nonenal, Oxidized LDL
* P-Hydroxyphenyllactate, Homogentistate
* ROS production, Neutrophil mediated oxidative burst, antimicrobial mechanism, Increased oxidative stress associated with infection including H pylori, prevotella intermedia and Brucella melitensis
o P-Hydroxyphenyllactate
| o Homogentistate
106
(pp. 523-531) Note the array of biomarkers that can reveal the status of: Pathogen Invasion
* 3-nitrotyrosine (3NT), Methionine sulfoxide
* DNA strand breakage (comet assay)
* Malondialdehyde (lipid peroxides), Isoprostanes, 4-hydroxy-2-Nonenal, Oxidized LDL
* P-Hydroxyphenyllactate, Homogentistate
* ROS production, Neutrophil mediated oxidative burst, antimicrobial mechanism, Increased oxidative stress associated with infection including H pylori, prevotella intermedia and Brucella melitensis
o ROS production
o Neutrophil mediated oxidative burst, antimicrobial mechanism
o Increased oxidative stress associated with infection including H pylori, prevotella intermedia and Brucella melitensis
107
(p. 591) What advantage may be derived from the use of a patient’s genomic data when choosing drug therapies, in terms of CYP450?
• (p. 591) A patient with low or absent activity in a CYP450 activity needed to clear a drug can develop overdose effects when standard dosing schedules are used. Also, some drugs produce their effects only in individuals with specific isoforms of cell components. In many such instances, genetic testing can inform about the individual variants.
108
(Fig 11.2) What information does the term (C677T) convey about a SNP?
• (Fig 11.2) The term (C677T) specifies that exact location (base number 677) and nucleotide replacement (cytosine to thymine) that is present.
109
(Fig 11.3) From information about estrogen hydroxylation in Fig. 10.7 on p. 567, what proportion of drugs are metabolized by the cytochromes uniquely required for forming 16a-hydroxyestrone?
* CYP3A4 and CYP2E; 35% and 4%, respectively.
* CYP3A4 and CYP2E; 4% and 35%, respectively.
* CYPA1 and CYP2E; 35% and 4%, respectively.
* CYPA1 and CYP3A4; 4% and 35%, respectively.
• (Fig 11.3) The CYP3A4 and CYP2E variants required for 16a-hydroxyestrone formation are present at 35% and 4%, respectively.
110
(Fig 11.4) Which steps in the overall process from DNA expression to cellular outcome are potentially impacted by environmental factors?
• (Fig 11.4) All steps of DNA transcription, RNA translation and protein function are potentially impacted by environmental factors.
111
four main urea cycle intermediates (NOT OAs)
| COAA
citrulline, ornithine, arginine, argininosuccinate
112
- Gly and Ser are related by a single reaction that transfers the _______ _________
- they normally move __ and ____ together on amino acid profiles.
hydroxymethyl group,
| move up and down together
113
(Fig. 5.2) Since specimen collection for both serum triglycerides and plasma fatty acids is done in the _______ ____, the circulating form of lipoprotein is largely ___ particles.
* fasting state, LDL
* fasting state, VLDL
* fed state, LDL
* fed state, VLDL
fasting state
| LDL
114
what does HHH stand for?
* hyperammonemia , hyperargininemia, hypertrophy
* hyperammonemia, hyperarganinemia and hyperornithinemia
* hyperglycemia, hyperarganinemia and hyperornithinemia
* hyperlipidemia, hyperammonemia, hyperargininemia
hyperammonemia, hyperarganinemia and hyperornithinemia
115
urea cycle effects due to low ornithine may be corrected with what supplementation?
* Arg
* Phe
* Tau
* Met
arginine
116
T for F: There is a requirement to perform a 2-carbon removal from the carboxyl group end of the 24:6n3 intermediate that is not possible inside mitochondria.
true
117
The _____ intermediate must be transported out of the mitochondria and into the peroxisomes in order to generate ___ that is critical for infant brain development.
* VLCFA, DHA
* VLCFA, EPA
* LDL, DHA
* LDL, EPA
VLCFA, DHA
118
18:3n3
α-linolenic (ALA)
119
T or F: peroxisomes increase in response to dietary lipids, hormones, toxicants and drugs that bind to nuclear regulatory proteins (______)
f: decrease in response
| PPAR
120
Activation of PPAR-α reduces ________ level and is involved in regulation of energy homeostasis.
triglyceride
121
When fish oil supplements are used excessively, the superior binding of the n-3 fatty acids to desaturase enzymes tends to suppress the desaturation of _1_and _2_ to form _3_, casing potentially clinically low levels of _3_.
of linoleic and GLA to form AA,
122
Since peroxisome proliferation is a fundamental cellular response to energetic and immunological stressors, any condition that might require those systems may be impacted by deficiencies of PUFAs or _______.
* Vitamin A
* Vitamin C
* 9-cis- retinoic acid
* Ascorbate
• Vitamin A
123
Table 5.5) Highly diverse symptoms have been found in linoleic acid deficiency because of its central role in two processes that broadly impact cellular function. They are 1) cell membrane properties that affect membrane-bound protein complexes and receptors in all tissues and 2) formation of the dominant eicosanoid precursors, ___ and __.
GLA and AA.
124
(CI 5.7) The etiology of adrenoleukodystrophy is lack of ________ activity required for oxidation and clearance of ______. Those fatty acids accumulate massively, producing chronically progressive neuropathic symptoms in the patients.
peroxisome
| VLCFA
125
(pp 360-361) Aggressive _______ _ therapy may help to reduce elevated p-hydroxyphenyllactic acid and the concomitant elevated cell division rate stimulation that tends to produce systemic oxidative stress.
* Selenium
* vitamin A
* vitamin C
* vitamin E
vitamin C
126
Maple syrup urine disease: High doses of what essential nutrients are helpful in certain forms? Why don’t all forms respond to the nutrient supplementation?
Raising cellular levels of thiamin, riboflavin, niacin, pantothenic acid (B1, B2, B3, B5) and lipoic acid may restore the enzyme activity.
If the genetic polymorphism causes severe alteration in enzyme binding sites for the cofactors, the raising their concentrations may have no effect.
127
What condition is associated with the polymorphism in the glycine cleavage system?
If various evaluations indicate normal levels of those vitamins,..... non-ketotic hyperglycinemia.
128
citrate, cis-aconitate, isocitrate, alpha, ketoglutarate, succincate, fumarate, malatea, hydroxymethylglurate,
are markers of what?
CAC markers
129
what are adipate, suberate, etymalolanate ?
* detoxification
* dysbiosis
* neurotransmitters
* oxidative damage
* carbohydrate metabolism
* the markers of FA oxidation
the markers of FA oxidation
130
pyruvate, lactate, and beta hydroxybutyrate are markers of____?
* detoxification
* dysbiosis
* neurotransmitters
* oxidative damage
* carbohydrate metabolism
* the markers of FA oxidation
carbohydrate metabolism
131
beta - hydroxyisovalerate is a maker for what?
biotin
132
xanthurenate can indicate need for what vitamin?
B6
133
What are the markers for neurotransmitters? (5)
vanilmandelate, homovanillate, 5-hydroxyindolacetate, kynurenate, quinolinate
134
vanilmandelate, homovanillate, 5-hydroxyindolacetate, kynurenate, quinolinate are the markers for what?
* detoxification
* dysbiosis
* neurotransmitters
* oxidative damage
* carbohydrate metabolism
* the markers of FA oxidation
neurotransmitters
135
markers of oxidative damage? (2)
p-hydroscyphenyllactate and 8-hydroxy-2'-deoxyguanosine (8-OHdG)
136
what are the detoxification makers (6)
2-methylhippurate, orotate, glucarate, alpha- hydroxybutyrate, pyroglutamate, sulfate
137
2-methylhippurate, orotate, glucarate, alpha- hydroxybutyrate, pyroglutamate, sulfate are marker for what?
* detoxification
* dysbiosis
* neurotransmitters
* oxidative damage
* carbohydrate metabolism
* the markers of FA oxidation
detoxification
138
p-hydroscyphenyllactate and 8-hydroxy-2'-deoxyguanosine (8-OHdG) are markers for what?
* detoxification
* dysbiosis
* neurotransmitters
* oxidative damage
* carbohydrate metabolism
* the markers of FA oxidation
oxidative damage
139
benzoate, hippurate, phenylactate, phenylpropioante, p-cresol; p-hydroxybenxoate, p-hydroxyphenylacetate, tricarballyate, d-lactate, 3,4, dihdroxyphenylpropionate, d-arabinitol
are markers for?
* detoxification
* dysbiosis
* neurotransmitters
* oxidative damage
* carbohydrate metabolism
* the markers of FA oxidation
dysbiosis
140
When fish oil supplements are used excessively, the superior binding of the n-? fatty acids to desaturase enzymes tends to suppress the desaturation of linoleic and GLA to form __, casing potentially clinically low levels of __.
3, AA
141
Clostridia, Enterobacter and Bacillus spp. are markers of?
* candida
* ammonuria
* hypertension
* hepatic detoxification
(Table 7.5) The ammonuria indicated by elevated orotate in CI 6.7 suggest that bacteria genera capable of high ammonia production are abundant, including
142
(pp 364-365) Urinary glucarate is a marker of increased ______ _______ system activity. It is a by-product of pathways leading to glucuronic acid formation. Oral glucarate is not helpful for assisting hepatic detoxification or for relieving potential elevated rates of intestinal bacterial glucuronide hydrolysis.
hepatic detoxification
143
T or F: Oral glucarate is helpful for assisting hepatic detoxification or for relieving potential elevated rates of intestinal bacterial glucuronide hydrolysis.
FALSE: glucarate is NOT helpful in hepatic detox
144
In the vitamin B6 sufficient state, however, inflammation produces increased activity of the kynurenine pathway in the brain where the products that accumulate most often are ______ and ______ because brain tissue does not express the enzyme required to complete the conversion to nicotinic acid.
* homovanillate and quinolinate
* quinolinate and Picolinate
* quinolinate and vanilmandelate
* vanilmandelate and Picolinate
quinolinate and Picolinate
145
True or False: 16a-hydroxyestrone is an estrogen antagonist and 2OHE1 is an estrogen agnoist.
FALSE: 16a-hydroxyestrone is an estrogen agnoistand 2OHE1 is an estrogen antagonist.
