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1 May 2019

In personal Health:

"I'm so fat!" How many times have you heard that comment? How does it make you feel when "thin" people say they're fat? Does it send a different message when overweight/obese people make the same comment? How could you help a friend who is overweight/overfat who constantly makes such comments, but never seems to do anything about it? What would you say to a "thin" person making the same comment?

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Beverley Smith
Beverley SmithLv2
3 May 2019

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First of all I am not endorsing Intelligent Design (Wikipedialink); I'm asking this because I (someone who does not have abackground in biology, organic chemistry, or philosophy) got into aconversation with someone who does endorse it, and I'm trying tosee his point of view as far as rationality can allow. Second ofall, I apologize for any vagueness; Intelligent Design isn't wellenough defined as a theory for me to help that. I also apologize ifthis is rehashing content already plentiful on the Internet, butfor my purposes I can't simply depend on the likes of Wikipedia orTalk Origins, so what I'm looking for here instead is to take theopposite approach and see, based on your informed minds, if therecould possibly be any reasonable likelihood of an ideal ID theorybeing adopted.

I'm looking for the most favorable consideration for what IDmight be if it were best developed as a viable hypothesis or theoryto get an idea of how far such a discussion is worth taking. Anunbiased, informed Devil's advocate, if you will.

My cursory investigation of what Stephen Meyers (video link) andMichael Behe (video link) say (correct me if I'm wrong) seems to bethat either the first cell was likely designed intelligentlyjudging by the complex code of DNA and that evolution took coursefrom there, or that the first cells were made and many instances ofevolution were from some kind of intelligently guided mutations aswas needed to make "irreducibly complex" cells or body functions(whether the guidance stops after the Cambrian or continued even tothe point of making different types of new bacteria and differenttypes of apes/humans or whether every single mutation and adaptiveability is being guided, I'm not sure if they're at any consensus,and that's why I don't know if I should stop my question atabiogenesis or include evolution). The person I spoke with alsobrought up some specific claims (everything looks designed, DNA hasordered, complex information, blood clotting is irreduciblycomplex, ID can and has make predictions like decades ago that"Junk DNA" wasn't junk) that I don't need you to debunk (I haveGoogle).

But if there could be any possible support or truth to any ofthe above, I would appreciate knowing about that. (Again, Devil'sadvocate so I can be informed and understand where the points comefrom.) Reading an ID book alone, it would be in places hard to knowwhere they differ from actual scientific conclusions. After all,when someone who seems to know what they're talking about and canexplain something in technical detail says that something isimpossible or extremely unlikely, it's hard for me to know why theywould be wrong (are they ignoring other possibilities?misrepresenting facts? are they really right and just getting thecold shoulder from an atheistic scientific community because itimplies a deity?). So I focus on mainstream sources, even if theydon't bother entertaining ID and leave me ignorant of its possiblevirtues. And thus I'm hoping someone from this informed communitymight enlighten me to what those possible virtues might be.

1. How does prenatal body weight influence theamount of weight a woman should gain during pregnancy?

2. At what week of gestation does the embryonicperiod begin? When does the fetal period begin? When is the mostlikely time a teratogen can do the most damage, during theembryonic or fetal period?

3. What risks are there to a baby if the mothergains too little weight during the pregnancy? What risks are thereto a baby if the mother gains too much weight during thepregnancy?

4. What is the relationship between mercury,fish and pregnancy?

5. What are some of the common gastrointestinaldistresses pregnant women experience? What remedies are availableto manage them?

6. What is fetal alcohol syndrome? How can itbe prevented? When can it be most accurately diagnosed?

7. How does the MyPlate food guidance systemsupport a healthy pregnancy?

8. Why is a prenatal dietary supplementrecommended throughout pregnancy?

9. What benefits are there to exercising duringpregnancy? How should exercise be modified during eachtrimester?

10. What is one of the best ways to trackgrowth in children? What are you looking for when you trackgrowth?

11. What benefits to the infant are provided bybreastfeeding?

12. What benefits to the mother are provided bybreastfeeding?

13. What nutrients are vital for supportingdental health in infants and children?

14. Although breast milk has advantages overformula, breastfeeding not recommend if the nursing mother haswhich conditions?

15. At what age is it safe to switch fromformula or breast milk to cow’s milk?

16. Which solid foods should be introducedfirst and at what age and why: cereals, vegetables, andfruits?

17. Do infants have the same AMDRs as adults?If not, how are they different? Is the grams/kg body weight forprotein higher or lower for an infant compared to a teenager oradult?

18. Does eating sugary foods lead tohyperactivity in children? If not, what does?

19. What is the division of responsibilitybetween caregivers and children for feeding?

20. How would you outline a healthy dailyschedule and meal/snack pattern to follow for a preschooler and aschool-aged child?

21. Can the MyPlate tool support childhoodnutrition? How? What other tools can be used?

22. What are the consequences of obesity inchildhood? How can childhood obesity be prevented?

23. How can food allergies be prevented andmanaged in childhood?

24. The rapid weight gains that girlsexperience during adolescence begin at what ages? Forboys?

25. Are the AMDR guidelines for adults the sameas for teenagers? What are these guidelines? (Percent calories fromfat? Carbohydrate? Protein?)

26. Why are calcium and iron the most importantminerals for teenagers? Does gender make a difference?

27. If teens are overweight and it isunrealistic to believe they will grow into their current weight?What rate of weight loss is recommended in terms of pound(s) perweek?

28. Describe the typical diets of teens thatsmoke?

29. What is the nutritional consequence alcoholfor teens?

30. Adolescences should be physically activefor how many minutes/day?

31. How does body composition change over theyears? Is there anything one can do to affect this change?

32. Does Basal metabolic rate increase ordecrease with age? Why? Will the elderly need more or fewercalories per kilo body weight than those who are middleaged?

33. Do the elderly need more or less fluid percalorie intake than younger adults? Why?

34. If an elderly person has osteoporosis, canhe or she do anything to improve this condition?

35. How can a poverty-stricken older adult beassured of eating healthy meals on a regular basis?

36. Why is exercise important for theelderly?

37. How many calories are there in a gram ofalcohol? Why does consuming 2 alcoholic drinks in a man has thesame physiological affect as one drink for a woman?

38. What practices will decrease the rate ofalcohol absorption into the blood?

39. Define moderate alcohol intake in terms ofdrinks per day for men and women and say how it relates to HDLcholesterol.

Roger Maxwell is very health-conscious. He runs, swims, and hikes; follows a lowcarbohydrate diet; and generally feels great. He sees a physician when he needs to, in addition to annual physical exams at the large company where he is an engineer. He'd never allow himself to get so out of shape that heart disease would be a risk. Because of his strict adherence to this healthy lifestyle, Roger is surprised when a medical intern, gazing at his yearly elecfrocardiogram (ECG) at his work physical, clearly picks up on something.

"What? What are you looking at?" Roger blurts out while buttoning up his shirt.

"Oh, it's probably nothing." But she doesn't look like it's probably nothing.

"The heart murmur? My mom's been telling me about it since childhood. Not a big deal. The doctors called it something last year, something I never heard of." "Did you check it out?" asks the intern.

"Nah. It wasn't bothering me, so I forgot about it. Why? What's wrong?"

"Well, maybe you should ask the doctor to explain it again and suggest what to do."

"About what?"

"The doctor will explain it. Please don't worry, though," says the intern as she rushes off to the next patient.

Roger's electrocardiograms had in fact been showing that he has had long QT syndrome, and not a heart murmur, for many years. The doctor explains that this is a problem with the heart's rhythm, and not its valves. Roger goes home and Googles long QT syndrome right away. What he finds concerns him enough to alert his relatives.

Long QT syndrome is a lengthening in the time that it takes the ventricles (the lower two heart chambers) to recover after a contraction, called the QT interval on an electrocardiogram. This delay is called torsade de pointes, and it causes lightheadedness upon standing or even fainting, as blood pressure drops when the heart rhythm becomes abnormal. If the arrhythmia turns into the more erratic condition called ventricular fibrillation, it can be deadly. Some cases •of sudden cardiac arrest in people who apparently do not have heart disease are in fact due to long QT syndrome. This 'may have been the case with Roger's aunt, Amelia, his mother's sister, who died at age 34 of what was thought to be a heart attack, but, now Roger realizes, was more likely an arrhythmia. Still, with only one affected relative, Roger had never thought of his aunt's •early demise as a family history, especially since his mother is healthy.

Roger reads that in people with some forms of long QT syndrome, fatal arrhythmia can be triggered by intense emotions or a sudden loud sound. The first recorded case of the condition was a little girl, who collapsed dead •when her teacher suddenly yelled at her. Her older brother had died in a similar circumstance. Suddenly, Roger remembers that his daughter Sheila faints very easily. She even passed out once at a rock concert because she got so excited. He'd never panicked over it because his mother fainted easily, too. A pattern was emerging.

Long QT syndrome is caused by mutations in any of at least 10 genes that encode either proteins that form parts of ion channels (potassium, sodium, or calcium) or proteins that affect the functioning of these channels. Ion channels control the spread of nerve impulses and the resulting muscle contraction. The time for the heart's reeovery after a beat, called repolarization, extends the period when ions are trapped inside heart muscle cells because the channels are blocked, too slow to open, or too quick to close in people who are at elevated risk due to inheriting a mutation. People with long QT syndrome can experience arrhythmia if they take certain drugs that prolong the QT interval. These drugs include certain antibiotics, antidepressants, and diuretics ("water pills").

Roger reads about the different genes and drug combinations that cause long QT syndrome on Wikipedia, and then he scans www.genetests.org to find labs that test for all of them. Only then does he make an appointment with a cardiologist, and he arranges to have his blood and that of his daughter and mother sent to one of the labs. Two weeks later, he learns that they all have a dominant mutation in a gene called HERG (for "human ether-a-go-go") that causes long QT syndrome type 2 (LQT2). Even healthy family members could have inherited the mutation, because 15 percent of people with long QT syndrome do not have symptoms. The concern is their increased risk of developing symptoms in the future—perhaps suddenly.

Question 1 : Roger is upset that in the past doctors had not been more insistent that he follow up on the abnormal ECG pattern. When he mentions this to his primary care physician, she answers, "I didn't say anything because you are so healthy, and people who have cardiac arrest from long QT do so in young adulthood. You're too old to worry about it." But Roger should be worried, because

a. he looks younger than he is, so could still be at risk

b. the condition can be inherited, so others in the family could be affected.

c. he could die at any time.

d. he can no longer take antibiotics.

e. long QT syndrome can cause cholesterol to build up in his coronary arteries.

2. Individuals who should take genetic tests for long QT syndrome are

a. all the people in generation IV.

b. Eric, Joan and Peter, and then Dylan, Anika, Sean, Keri, and Anna if a parent has the mutation.

c. Juanita, Larry, Joan, Peter, and Ellie.

d. Abe, Sara, Craig, Philip, Edwin, and Yvonne.

e. Only those who are athletic.

3. The mode of inheritance of long QT syndrome in the Maxwell family is

a. X-Iinked recessive

.b. autosomal recessive.

c. autosomal dominant.

d. sex-limited.

e. X-Iinked dominant.

4. Some people who inherit the same mutation as Roger do not experience any symptoms. This means that the mutation is

a. variably expressive.

b. genetically heterogeneic.

c. polygenic.

d. incompletely penetrant.

e. dominant.

5). The fact that mutations in any of several genes can cause long QT syndrome means that the condition is

a. variably expressive.

b. genetically heterogeneic.

c. polygenic.

d. incompletely penetrant.

e.recessive.

6). The risk that Sean, Keri, or Anna has inherited the family's mutation for long QT syndrome is

a. 1

b. ¾

c. ¼

d. ¼

e. 1/8

7) Roger is relieved that he does not have- LQT7, which affects skeletal as well as cardiac muscle, causing short stature and scoliosis. He is also glad that he doesn't have LQT8, which causes many symptoms, or either of two types that also cause deafness. These other forms of the condition, with more than one symptom, exhibit

a. invariable expressivity.

b. complete penefrance.

c. genetic homogeneity.

d. pleiotropy.

e. phenocopy.

8) The reason that mutations in different genes all cause the same phenotype of extended QT interval on an ECG is that

a. the heart is an extremely complex organ.

b. the genes all encode proteins that affect ion channels essential for maintaining heartbeat.

c. the genes all encode the same protein.

d. the mutations all affect the genes in the same way.

e. the QT interval is highly variable, even within individuals at different times.

9). A phenotypic pattern in a family that could be due to inherited long QT syndrome is

a. sudden cardiac death in one or more young people and individuals who faint easily.

b. many individuals who eat a very fatty diet and are sedentary but do not develop heart disease.

c. many individuals with hypertension.

d. many individuals who suffer heart attacks after age 50.

e. a family with rnany athletes who have very low heart rates because of intense and frequent exercise.

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