Suing your children in Singapore

In the post I wrote yesterday I referred to the tradition of filial piety in Singapore. When I was discussing that topic with a lawyer at the Centre for Biomedical Ethics he told me about Singapore's fascinating "Maintenance of Parents Act," which went into effect in 1996.

The law allows any Singapore resident, 60 years old and above, who is unable to maintain himself adequately, to claim maintenance from his or her children, either in a lump-sum payment, or in the form of monthly allowances. If the parent gives consent, relatives or caregivers may apply for court action on the parent's behalf. Cases (recently there have been about 100-150 per year) are heard by a special Tribunal that decides whether payment should be made and how much it should be, based on criteria including the parent's financial needs and the child's earning capacity and other financial obligations.  The maintenance claim may be dismissed if the children can prove that they were abused, neglected or abandoned by their parents when they were young. The law stipulates that only the basic amenities and physical needs of the applicant including shelter, food and clothing are required.  The maintenance is not linked to the parent’s previous standard of living.The applicants tend to be Chinese fathers, either widowed or divorced.
The law was proposed by Walter Woon, who was a member of the Singapore Parliament at the time and also professor of law at the National University of Singapore.I found his comments about the law very persuasive, and quote them here:

Some critics have said that applying to the court for maintenance from one's children is undignified. I wonder whether it is more dignified to apply for public assistance or to depend on the kindness of strangers. Or perhaps it would be more dignified to starve quietly and without fuss.

Cynics have dubbed this the 'Sue Your Son' law. They miss the point completely. It would be only in a very extreme case that any parent would take his children to court. The effect of the bill, if it becomes law, will be more subtle.

First, it will reaffirm the notion that each individual has a responsibility to look after his parents. It is not society's responsibility. Singapore is still conservative enough so that this idea is not objectionable to most people. The bill reinforces the traditional values of Christianity, Islam, Hinduism and Buddhism as well as Confucianism. It doesn't hurt a society now and then to be reminded of what its core values are.

Second and more important, it will make those who are inclined to shirk their responsibility think twice. As things stand, If a person asks family members or clergymen or the Ministry of Community Development to help him get financial support from his children, the most that they can do is to try to mediate. The trouble with mediation is that the mediators have no teeth. They can exhort, preach, persuade, cajole, plead and even beg. But when push comes to shove, there is currently no way that a son can be forced to support his parents.

But if there were a legal remedy, that would be a different matter. To be sued by one's parents would entail a massive loss of face. It would be a public disgrace. The hand of the conciliator would be immeasurably strengthened. It is far more likely that some sort of amicable settlement would be reached through private mediation if the recalcitrant son knows that the alternative is a public trial. So, one hopes that the fact that such a law exists will make it unnecessary for it to be invoked.

The critics who say that the proposed law does not promote filial piety are right. It has nothing to do with filial piety. It kicks in where filial piety fails. The law cannot legislate love between parents and children and husbands and wives. All the law can do is provide a safety net where morality proves insufficient.

I take a pragmatic view. The law I have proposed won't affect the people who already are supporting their parents, not only with money but, it is hoped, with love and respect. The only ones who need worry are those who aren't living up to their moral obligations. If the law helps even one poor person, I think the effort is worth it.

Many years ago, in what turned out to be the last year of my father's life, I persuaded him to move from Florida to Massachusetts, where I live. He was blind from macular degeneration and needed a supportive living environment - ultimately one with 24 hour nursing care available. I engaged a geriatric care manager to help me (his only child) scope out the options. She told me about maneuvers that would allow him to receive Medicaid support. In the spirit of Professor Woon, I did not want to do that. The care my father  needed was costly, but I could afford it, and it seemed obviously wrong to ask my fellow citizens to support him. If I had refused to pay for his support I hope Medicaid would have come after me, as Professor Woon wanted the Singapore authorities to be able to do.

Setting Limits Fairly in Singapore (2)

I wrote a post yesterday  before I led a workshop for ethics committees or hospital personnel simply interested in the ethics of setting limits in health care . Today I want to write about what I learned from the 25 wonderfully engaged folks I met with and from conversations subsequent to the workshop. Here are my initial observations:

1. One of the three core components of the framework for setting limits fairly that Norman Daniels and I developed is publicity or transparency. On the basis of our observations in the US, Canada, and the National Health Service in England, we argued that those responsible for setting limits (health plans, government agencies) should share the rationale for policies and decisions with the public. In liberal democracies in the west, this stipulation is widely accepted. My impression is that Singapore has more of a tradition of accepting governance by experts and judging their policies by results, without expecting the level of transparency, access and participation that is especially valued in the US. The group I spoke with suggested that the value we in the US place on transparency is not as strongly shared by the population and government in Singapore. To be useful, transparency requires a public experienced in understanding, evaluating, and interacting with policy makers, and policy makers experienced in a reciprocal role. My tentative conclusion thus far is that for transparency to contribute to improved policy making in Singapore, a period of learning or skill development will be required. I did not recommend a sudden shift in practice, but did suggest development of a strategy for how to engage the public in constructive interactions over time.
2. Physicians in the group told me that it's common for families to press for continued "treatment" even when the clinical staff has concluded that comfort care is the right approach. I asked them whether families doubted their clinical assessment or believed that a miracle might occur. Those weren't the reasons. They explained that there is a strong expectation of filial piety in Singaporean culture, and not pressing for continued active "treatment" felt disrespectful and even shameful to the family. They hoped that as advance directive conversations became better developed they will be able to talk with children about "what would your father/mother have wanted in this situation?" Their sense was that as is true in the US, most elderly people would want to shift to comfort care and not be "flogged" by fruitless interventions. Moving to comfort care could then be seen as the way to show true filial piety!
3. As part of our discussion of the family role in setting limits, a participant told us that because of family guilt if they feel they aren't doing "everything," talking with families about options that from a realistic perspective offer no benefit even though we can never say with absolute certainty that they won't be effective for the first time now can cause real harm to families. She described a situation in which a family sold its home to pay for an intervention that in practical terms was "futile."
4. Singapore health policy has been developed to minimize the risk of what they call the "buffet syndrome" - that full coverage creates "moral hazard" and will lead to excessive utilization. Their system of required savings to pay towards one's own (and one's family's) care is very cleverly engineered to confront Singaporeans with the cost implications of their treatment and, at the same time, to try to make sure that they have resources in their savings accounts to pay for their choices. But with an aging population, more chronic illness, and new technologies, middle class families are facing costs they can't reasonably meet. The group cited another instance where in order to finance valuable treatment a family had to sell its home and impoverish itself. This was consistent with what a taxi driver told me - "In Singapore you can die, but you can't be sick."

Because of its good population health outcomes and low public spending (between 4-5% of GDP) the Singapore health system has received great praise, especially from strong believers in the market and "skin in the game." But because of the high payment expectations it sets for its citizens it has been criticized by liberal believers in comprehensive coverage. From my meeting with the workshop participants, and from a subsequent meeting with officials in the Ministry of Health, I believe the praisers and the critics are both wrong. Singapore hasn't found a magic bullet that can be readily transferred elsewhere. But Singapore hasn't created a cold, uncaring system. They're struggling very thoughtfully with the problem every developed economy is struggling with - how to find the optimal combination of communitarian caring for the population with the individuals responsibility for his own health and for the cost of care for himself and his family. What I would praise and want the US to emulate is the combination of thoughtfulness, analytical clarity, and non-ideological deliberation about managing the dilemmas of modern health care.

Setting Limits Fairly in Singapore (1)

This afternoon I'm speaking to members of the ethics committee (and interested others) at Tan Tock Seng Hospital in Singapore. The hospital was founded in 1844 by Mr. Tan, a wealthy Chinese businessman, who donated $7,000 to found a hospital for the "diseased of all nations." It's a large hospital, with 460 emergency visits and more than 2,000 specialty clinic visits every day.

I've been asked to speak about "Accountability for Reasonableness," the framework for setting limits that Norman Daniels and I described in our book Setting Limits Fairly. From a combination of conceptual analysis and field work done in the U.S. at not-for-profit organizations like Kaiser Permanente, and in Canada and the UK, we concluded that health care limit-setting required a fair process, which the book explicated. The framework emphasizes the role of relevant reasons, transparency about policies and their rationales, and processes for appeal and revision.

The framework has been found useful in liberal western democracies like Canada, the National Health Service in England, and the Scandinavian countries that have universal coverage under publicly established budgets. Singapore is decidedly "first world" in its remarkable economic achievements since independence (1965) - its per capita GDP in 2011 was approximately the equivalent of US$50,000, and the unemployment rate was 2.1%. From talking with Singaporeans and reading, my impression of the society and its governance is that it is much readier to accept expert authority than the US and liberal western democracies.

The ethics committee has asked me to discuss the case of a middle aged man with severe rheumatoid arthritis, for whom a costly new medication has been recommended. In the US context there would be no question as to whether insurance would cover the medicine if the clinical reasoning behind the recommendation was sound. Any debate about coverage would be expected to be open to public scrutiny. From what I learned from my colleagues in rheumatology, a patient in his condition would expect to have access to the medication in the US, and would certainly expect  to be able to challenge a decision not to be given access.

But as a visitor here I'm acutely aware of what a terrible example the US sets as a health system. Our costs are strangling other important societal investments, and because of our out of control costs we've left 50 million to be uninsured. So while I'm proud of the work Norman Daniels and I have done on fairness, I'm agnostic about its relevance for another society with (a) different moral and political traditions and (b) excellent overall health outcomes. I'll be introduced as a visiting expert, but before meeting with a group that provides clinical care and is concerned with ethics, I feel more like a learner than like someone ready to pronounce the truth about setting limits in a society significantly different from my own.

Health Care in Singapore

I've had the good fortune to be invited by the Singapore Centre for Biomedical Ethics to do a week of teaching about health system ethics. Right now I'm at Heathrow airport in London, in between the Boston to|London and  London to Singapore legs of my trip.

Although there's been a lot of interest in Singapore among health policy cognoscenti, I'd been in the dark about the Singapore system until I started preparing for my visit. My impression thus far is that the People's Action Party, which has governed since independence in 1965, sees health care as (a) a crucial contributor to well-being but (b) largely an individual responsibility to provide for oneself and one's family, and (c) not a right the state is responsible for fulfilling.

When Singapore became independent in 1965 it was impoverished, with a life expectancy of not much more than 60. The government's initial emphasis was on the determinants of population health - housing, clean water, jobs, and education. On the basis of their vigorous action, health and mortality improved markedly. In 1984 they introduced a mandatory medical savings account program - "Medisave" - in which all working people, including the self employed, contributed 6-8% of income to their "Central Provident Fund" account, to be used for their own medical care and for family members (spouse, children, parents and grandparents). In the 1990s the government introduced an insurance scheme ("Medishield") and a means tested fund for low income folks ("Medifund"). But there's still a very strong emphasis on individual responsibility and paying a fair share of the cost, even for the poor. (For information about the Central Provident Fund and the system of "3 Ms", see here .)

I've been told the Singaporean government sees "insurance" in a negative light. "Insurance" connotes dependency on the state and abdication of personal responsibility. In the U.S. the frequent comment that our health system is so out of control because the population lacks "skin in the game" comes from the same moral and economic perspective. As a dyed in the wool liberal I'm a staunch believer in a universal system - either something like Medicare for all or guaranteed access to strictly regulated health plans. The framework of values in Singapore is jarring for me, but their outcomes appear to be terrific, in terms of health indices and a much less costly system than we have in the U.S.

Since I recurrently criticize conservatives for what I describe as their "theological" commitment to market solutions, to be consistent I have to challenge my own liberal theology on this visit to Singapore. Stay tuned

Protein, Gluconeogenesis, and Blood Sugar

Recently (for some conception of recent) we asked the question: If You Eat Excess Protein, Does It Turn Into Excess Glucose?

One of the potentially confusing aspects of this question, is the difference between gluconeogenesis (GNG) — the creation of new glucose that didn't exist before, and increases in blood sugar. In response to our post, several people made comments that indicated an implicit assumption that changes in blood sugar can be used as a measurement of GNG, but as we will explain below, this is not the case. However, it brought to our attention an important distinction.

There are several reasons people might care about excess GNG. One we have already addressed: It is not the case that GNG requires excess cortisol.

In terms of the effect of the glucose itself that results from GNG, there are two distinct concerns:

• How does excess GNG affect blood sugar levels? Blood sugar levels are important because too much sugar in the blood at a given time can cause damage to cells ⁰.
• Does producing more glucose via GNG ultimately lead to either using more glucose for fuel, or storing it as fat?

So when people worry about protein causing excess GNG, what they are really worrying about is that protein will adversely affect their blood sugar levels, or that they are going to use more glucose for fuel than they intended, or that they will store it as unwanted fat.

While it would be interesting to understand the effect of eating excess protein on GNG, it doesn't directly address those underlying questions, because there are many other mechanisms in play. We want to know whether for ketogenic dieters eating excess protein adversely affects blood sugar levels, whether it leads to higher consumption of glucose for fuel, and whether it increases the tendency to store fat.

In this article, we will directly approach the first of these questions.

In Brief:

• Because the level of sugar in your blood depends on how much is coming in (and there is more than one source), and how much is going out, changes in blood sugar cannot by themselves tell us about the rate of GNG.
• Nonetheless, when we wrote the original article suggesting that eating excess protein was unlikely to result in an increased rate of GNG, one of the assumptions we made was that eating protein does not raise blood sugar. We made this assumption because it is true in non-diabetic, non-ketogenic dieters. However, we have recently learned that this is not true in ketogenic dieters.
• In response to protein, blood sugar rises on a keto diet, even though I/G — the ratio of insulin to glucagon, stays constant, whereas on a glycolytic diet, I/G rises, but blood sugar stays constant. There is evidence that I/G is tightly correlated with glucose production, so this is suggestive that in keto dieters glucose production is not affected by eating protein. However, we lack direct experimental evidence.
• Although blood sugar rises in keto dieters eating protein, it stays within safe bounds, at least in our experience, and in the experiment we looked at.

What affects blood sugar?

Fundamentally, the amount of sugar in the blood at any given time depends on two things: how much is coming in, and how much is going out. On the input side, blood sugar can come from three sources:

• We can eat carbohydrates, and have sugar enter the blood through digestion.
• We can make glucose out of glycogen (the limited amount of glucose stored in persistent form in the liver). This process is called glycogenolysis.
• Thirdly, we can produce new glucose by GNG.

Note that because of glycogen storage, it is possible for sugar to enter the blood that has not come directly from GNG. Even on a keto diet, there is still a substantial proportion of glucose production from glycogenolysis. Ultimately, of course, the glycogen in keto dieters also comes from GNG that happened previously.

On the outgoing side, the rate of sugar leaving the blood can also change depending on the uptake by cells. It can be used for fuel, stored as fat, or turned into glycogen for storage (glycogenesis).

This means that changes in blood sugar can happen in either direction, without us being able to conclude anything about the rate of GNG. Therefore, observations about increases in blood sugar in response to protein are not conclusive evidence about GNG.

The effect of protein on blood sugar

It is well established that under typical test conditions protein ingestion does not significantly effect blood sugar levels, either alone ¹ or in combination with other foods ². This graph shows the typical response to glucose (solid line) and protein (dashed line) ingestion in two non-diabetics after an overnight fast ³:

Of course, the “typical conditions” in those experiments did not include keto dieters.

However, there was an experiment in 1971 that did test the blood glucose response to protein in people who had restricted carbohydrates to ketogenic levels for one week, and compared it to the values after reintroducing carbohydrates for a week ⁴. The group size was small, and the keto-adaptation time was short, but nonetheless, the results showed that blood glucose did in fact rise in the keto dieters ingesting protein. The experimenters also measured the blood levels of the blood sugar regulating hormones insulin and glucagon and their ratio, I/G.

There is evidence that it is I/G, and not the absolute levels of either hormone, that ultimately regulates glucose production ⁵,⁶,⁷,⁸.

Interestingly, in the keto dieters, although the levels of these hormones significantly changed, their ratio did not.

Here is a summary of the results:

Diet type	Fasting				After Protein
	glucose	insulin	glucagon	I/G molar ratio	glucose	insulin	glucagon	I/G molar ratio
Ketogenic	78 +/- 3	8 +/- 2	128 +/- 17	1.7 +/- 0.3	90 +/- 3	15 +/- 4	218 +/- 10	1.83 +/- 0.4
Glycolytic	94 +/- 5	17 +/- 4	87 +/- 15	4.35 +/- 1.38	"baseline or lower"	28 +/- 14	167 +/- 13	8.2 +/- 4.66

In response to protein, blood sugar rises on a keto diet, even though I/G stays constant, whereas on a glycolytic diet, I/G rises, but blood sugar stays constant.

Because the number of subjects was small, the authors emphasize that this study cannot give us precise estimates of the numerical values of blood sugar (or hormones) in response to protein. It can only tell us that this rise in blood sugar happens qualitatively. In other words, they've shown that a rise in blood sugar happens, but we can't be sure that the average rise is going to be 10 mg/dL if we tested a lot more people.

It is important to understand that this is not a very complete picture. For example, it doesn't show whether there is a relationship between how much protein is eaten and blood sugar. It could be, for example, that any amount of protein results in the same increase in blood sugar. It could be that protein ingestion results in a small rise in blood sugar with a duration that depends on the amount of protein. It could be that eating protein on a keto diet causes your blood sugar to rise steadily according to the amount of protein eaten until it reaches some maximum value, such as a 20 point rise, after which no further amount of protein has an effect. What is very unlikely is that the amount of protein has an unlimited effect: we would not expect, for example that if eating 50g of protein caused a 10 point rise, then eating 300g of protein would cause a 60 point rise. There is still a lot to learn here.

Note: Incidentally, these experiments would be easy for any of us to do at home. For example, you could get up after an overnight fast and measure your blood sugar. Then ingest 25g of protein, and measure your blood sugar every half hour until it returns to baseline to see how your blood sugar changes and for how long. Do that for three days, and then try it with 50g for three days. Then try 100g and then 200g. Use the same kind of protein in each case, like lean beef or egg whites (save the yolks for later!). Tell us what you find out.

One important conclusion from all of this, though, is that, at least at these protein levels, blood sugar stays in a safe range ⁹. There is good reason to be concerned about the level of sugar in your blood over the long term. We will write more about that in subsequent posts. For now we can simply note that the fasting level of blood sugar in this experiment was at the low end of the range considered optimal, and the rise in response to protein was well below the amount considered dangerous.

Acknowledgements:

This article was most spurred by a comment on the original article by Anna K. Thank you, Anna.

Once again, we are indebted to friendly correspondents for access to relevant scientific papers. This article was supported by friends in Windy City, Orlando, and Edinburgh. We couldn't have written it without you!

References:

⁰ Evidence type: summary of experiments
Campos C. Chronic hyperglycemia and glucose toxicity: pathology and clinical sequelae. Postgrad Med. 2012 Nov;124(6):90-7. doi: 10.3810/pgm.2012.11.2615.

(Emphasis ours)

Abstract

Type 2 diabetes mellitus (DM) is a progressive disease characterized by elevated plasma glucose levels. Type 2 DM results from a combination of factors affecting both peripheral tissue insulin sensitivity and β-cell function. A survey of the scientific literature on DM, glucose toxicity, hyperglycemia, nephropathy, neuropathy, reactive oxygen species, and retinopathy cited on PubMed/Medline from January 1975 to May 2011 was conducted. The relevant publications, chosen at the author's discretion, were used to synthesize this narrative review article. Chronic hyperglycemia imposes damage (glucose toxicity) on a number of cell types and is strongly correlated with the myriad of DM-related complications. Tissues most vulnerable to the effects of prolonged elevated plasma glucose levels include pancreatic β cells and vascular endothelial cells. The ensuing β-cell dysfunction promotes decreased insulin synthesis and secretion, further perpetuating the associated hyperglycemia. As for the vascular endothelium, chronic hyperglycemia is strongly correlated with many DM-related microvascular complications, including retinopathy, nephropathy, and neuropathy. The role of hyperglycemia in macrovascular complications is not well defined. Pathophysiologic modifications that arise in response to chronic hyperglycemia persist and may promote DM-related complications that manifest years later, even if plasma glucose levels have been brought under control. Increasing awareness of the mechanisms by which even modest hyperglycemia promotes long-lasting tissue damage highlights the need to achieve early tight glycemic control in patients with DM before substantial disease progression.

¹ Evidence type: review of experiments
Franz MJ. Protein: metabolism and effect on blood glucose levels. Diabetes Educ. 1997 Nov-Dec;23(6):643-6, 648, 650-1.

"Protein has a minimal effect on blood glucose levels with adequate insulin. However, with insulin deficiency, gluconeogenesis proceeds rapidly and contributes to an elevated blood glucose level. With adequate insulin, the blood glucose response in persons with diabetes would be expected to be similar to the blood glucose response in persons without diabetes. The reason why protein does not increase blood glucose levels is unclear. Several possibilities might explain the response: a slow conversion of protein to glucose, less protein being converted to glucose and released than previously thought, glucose from protein being incorporated into hepatic glycogen stores but not increasing the rate of hepatic glucose release, or because the process of gluconeogenesis from protein occurs over a period of hours and glucose can be disposed of if presented for utilization slowly and evenly over a long time period."

² Evidence type: experiment
José Galgani, Carolina Aguirre and Erik Díaz. Acute effect of meal glycemic index and glycemic load on blood glucose and insulin responses in humans Nutrition Journal 2006, 5:22 doi:10.1186/1475-2891-5-22

"When mixed meals are consumed, other food and macronutrients will be present. In this study, the results were similar to those observed in studies using isolated carbohydrates [6] and imply that other macronutrients had a negligible effect on the differential serum glucose and insulin responses. It has, in fact, been reported elsewhere that the amount and type of carbohydrate account for about 90% of the total variability in blood glucose response, whereas protein and fat in mixed meals scarcely contribute to the variance in blood glucose and insulin responses [1,2]."

³ Evidence type: experiment
Jerome W. Conn and L. H. Newburgh THE GLYCEMIC RESPONSE TO ISOGLUCOGENIC QUANTITIES OF PROTEIN AND CARBOHYDRATE J Clin Invest. 1936;15(6):665–671. doi:10.1172/JCI100818.

⁴ Evidence type: experiment
Walter A. Muller, M.D., Gerald R. Faloona, Ph.D., and Roger H. Unger, M.D. The Influence of the Antecedent Diet upon Glucagon and Insulin Secretion. N Engl J Med 1971; 285:1450-1454December 23, 1971DOI: 10.1056/NEJM197112232852603

⁵ Evidence type: experiment (non-human animal)
H.J. Seitz, M.J. Müller, W. Krone, W. Tarnowski Coordinate control of intermediary metabolism in rat liver by the insulin/glucagon ratio during starvation and after glucose refeeding: Regulatory significance of long-chain acyl-CoA and cyclic AMP. Archives of Biochemistry and Biophysics. Volume 183, Issue 2, October 1977, Pages 647–663

(Emphasis ours)

Abstract

The levels of serum insulin, glucagon, and free fatty acids (FFA) and the tissue concentrations of hepatic cyclic AMP, long-chain acyl-CoA (LCA), adenine nucleotides, inorganic phosphate, the intermediates of the Embden-Meyerhof pathway, the citric acid cycle (including acetyl-CoA and free CoA), and the cytoplasmic and mitochondrial redox couples were determined in the rat 12, 24, and 48 h after food withdrawal and 5, 10, 20, 40, 60, and 120 min after the refeeding of glucose. Using the measured metabolite contents in the liver, the alterations in the concentration of malate, oxaloacetate, citrate, and α-ketoglutarate and the changes in the energy state of the adenine nucleotide system and the redox state of the NAD system were attributed to the cytoplasmic and mitochondrial compartments by applying established calculation methods. Glucose refeeding provoked significant alterations in all parameters investigated. These changes occurred within minutes, reversing the hormone and metabolite pattern which had developed within 24 h in response to food withdrawal. Particularly, glucose refeeding resulted in a drastic increase in the insulin/glucagon ratio. Simultaneously, the level of serum FFA and the concentration of LCA in the liver declined. The latter alteration was accompanied by an increase in the cytoplasmic and a decrease in the mitochondrial ATP/ADP x P ratios. Moreover, the redox state of the cytoplasmic NAD system was shifted toward the oxidized state. When the appropriate data were plotted against each other, highly significant correlations were obtained (i) between the insulin/glucagon ratio and the serum FFA concentration, (ii) between the serum FFA concentration and the concentration of hepatic LCA, (iii) between the hepatic LCA concentration and the cytoplasmic energy state, and (iv) between the cytoplasmic energy state and the redox state of the cytoplasmic NAD system. These findings are interpreted to support the hypothesis derived from experiments carried out in vitro that the insulin/glucagon ratio via the FFA-dependent concentration of hepatic LCA might affect the translocation of adenine nucleotides between the cytoplasmic and the mitochondrial compartment, thereby regulating the cytoplasmic energy state and the redox state of the cytoplasmic NAD system, consequently. Glucose refeeding provoked rapid coordinate changes in the concentration of the intermediates of both the citric acid cycle and the Embden-Meyerhof chain, indicating the altered substrate flow through these pathways. Those metabolites, known to modulate the activity of key regulatory enzymes in vitro, were analyzed with respect to their suggested regulatory function. As to the established shift from pyruvate carboxylation to pyruvate decarboxylation after glucose refeeding, the data revealed that the decrease in pyruvate carboxylase activity can be attributed to the decrease in the intramitochondrial ATP/ADP ratio and the simultaneous fall in acetyl-CoA concentration, while the coordinate increase in pyruvate dehydrogenase activity can be ascribed to the decline in the concentration of LCA and, consequently, in the ratios of ATP/ADP , NADH/NAD, and acetyl-CoA/CoA within the mitochondria. As for the citric acid cycle, increased citrate synthesis from acetyl-CoA and oxaloacetate was supported by the rapid drop in the concentration of the established inhibitor of citrate synthesis, LCA. In contrast, the concentration of succinyl-CoA, an inhibitor of the enzyme in vitro, remained practically constant, questioning its regulatory function under the present experimental conditions. In addition to the activation of citrate synthase, the coordinate activation of isocitrate dehydrogenase was indicated by the LCA-mediated decline in both the mitochondrial ATP/ADP and the NADH/NAD ratios. Glucose refeeding immediately reduced urea excretion to basal values. This alteration was preceded by a drastic fall in the tissue concentration of cyclic AMP, supporting the physiological role of the nucleotide in the control of hepatic gluconeogenesis. In contrast, the observed changes in the concentration of the effectory acting metabolites (ATP, AMP, fructose 1,6-diphosphate, citrate, and alanine) were incompatible with the suggested function of these intermediates in switching over the substrate flow through the Embden-Meyerhof pathway from gluconeogenesis to glycolysis. The results are discussed in reference to the known rapid stimulation of fatty acid biosynthesis in the liver and to the transfer of reducing equivalents by the different shuttles of the inner mitochondrial membrane. In summary, it can be concluded that the insulin/glucagon ratio in a moment-to-moment fashion controls the glucose balance across the liver by regulating hepatic intermediary metabolism via the concentration of both LCA and cyclic AMP.

⁶ Evidence type: experiment (non-human animal)
Peret J, Foustock S, Chanez M, Bois-Joyeux B, Assan R. Plasma glucagon and insulin concentrations and hepatic phosphoenolpyruvate carboxykinase and pyruvate kinase activities during and upon adaptation of rats to a high protein diet. J Nutr. 1981 Jul;111(7):1173-84.

(Emphasis ours)

Abstract

Plasma hormones, glucose and free fatty acids, liver glycogen and two key enzymes of glycolysis and gluconeogenesis were examined in adult rats during a 40-day period of high protein feeding. Plasma insulin fell within 1 day but returned to normal after 4 days. Glucagon changed more slowly, reaching a maximum on day 4 and declined to near the control value within 24 days. Consequently, the insulin to glucagon ratio was lower on days 1, 4 and 8 and was nearly normal on day 24. With respect to hepatic enzymes, phosphoenolpyruvate carboxykinase activity rose sharply on the 1st day and remained elevated for 40-day period; the L-isozyme of pyruvate kinase, although unchanged on the 1st day, decreased thereafter and from day 8 on represented 15--20% of control. Circadian variations in these parameters were also measured in rats adapted to the high protein diet. In such animals, the diurnal change in plasma hormones was less marked but tended to be inverted with respect to controls; the insulin/glucagon ratio was highest during daylight on high protein and in late night on the control diet. Over 24 hours, pyruvate kinase activity was related directly and phosphoenolpyruvate carboxykinase inversely to the hormone ratio. We concluded that in rats adapted to high protein, as in controls, the diurnal balance between glycolysis and gluconeogenesis is probably regulated by the same factor, namely the insulin/glucagon ratio.

⁷ Evidence type: authority
Eric C. Westman, John Mavropoulos, William S. Yancy and Jeff S. Volek A review of low-carbohydrate ketogenic diets. Current Atherosclerosis Reports Volume 5, Number 6 (2003), 476-483, DOI: 10.1007/s11883-003-0038-6

The insulin/glucagon (I/G) ratio is a key determinant of lipolysis, glycogenolysis, and gluconeogenesis [14,15].

(We followed the references given for this assertion, and did not understand how they supported it, so we consider this evidence as authority-based, at least for us.)

⁸ Evidence type: in vitro experiment
S.R. Wagle. Interrelationship of insulin and glucagon ratios on carbohydrate metabolism in isolated hepatocytes containing high glycogen. Biochemical and Biophysical Research Communications. Volume 67, Issue 3, 1 December 1975, Pages 1019–1027

Abstract

The effect of physiological concentrations of glucagon and insulin on glycogenolysis was studied in the presence and absence of substrates in isolated hepatocytes containing high glycogen. In the absence of substrates glucagon stimulated glycogenolysis at 10−14M concentration, and addition of 100 μunits of insulin partially inhibited glucagon stimulated glycogenolysis (10−14M to 10−11M). However, in the presence of substrates, insulin completely inhibited glucagon stimulated glycogenolysis (10−14M to 10−11M), indicating that molar glucagon and insulin ratios control carbohydrate metabolism in liver. Additional studies showed incorporation of amino acid into protein was linear for only 3 to 4 hr in cells containing low glycogen, whereas in cells containing high glycogen, incorporation was linear for 8 to 10 hr.

⁹ Evidence type: authority
Postprandial Blood Glucose. doi: 10.2337/diacare.24.4.775 Diabetes Care April 2001 vol. 24 no. 4 775-778

Dissatisfying as it is, for now we will talk about safe as meaning not identified as correlating with current or subsequent development of diabetes.We will talk more about blood sugar in a subsequent post.

(Emphasis ours)

The word postprandial means after a meal; therefore, PPG concentrations refer to plasma glucose concentrations after eating. Many factors determine the PPG profile. In nondiabetic individuals, fasting plasma glucose concentrations (i.e., following an overnight 8- to 10-h fast) generally range from 70 to 110 mg/dl. Glucose concentrations begin to rise ∼10 min after the start of a meal as a result of the absorption of dietary carbohydrates. The PPG profile is determined by carbohydrate absorption, insulin and glucagon secretion, and their coordinated effects on glucose metabolism in the liver and peripheral tissues.

The magnitude and time of the peak plasma glucose concentration depend on a variety of factors, including the timing, quantity, and composition of the meal. In nondiabetic individuals, plasma glucose concentrations peak ∼60 min after the start of a meal, rarely exceed 140 mg/dl, and return to preprandial levels within 2–3 h. Even though glucose concentrations have returned to preprandial levels by 3 h, absorption of the ingested carbohydrate continues for at least 5–6 h after a meal.

Asparagus Basil & Rice Soup

I hope everyone is having a wonderful winter so far.  I know there are many lucky ones who enjoy summer weather all year long, but that is not the case here in Utah.  Up on our snowy mountain we have been lucky lately to hit 20 degree weather. So, between staying warm and healthy, this Asparagus Basil & Rice Soup does both and is as delicious as it gets!!  I started my recipe by soaking a cup of brown rice overnight in 3 cups of water with a tablespoon of apple cider vinegar. Drain and rinse rice before using in your soup.

 

Soaking your grains makes them healthier

Soaking rice is not as important as soaking other grains, but the texture that soaking produces is much nicer. The texture is more like white rice, and it becomes a more digestible grain.  The brown rice ‘flavor’ is a little less strong as well.  Research shows that, unlike white rice, brown rice still contains some of the germ or growth structure that actually resumes activity after soaking in water for 24 hours. This revitalization is helpful in normalizing metabolism when consumed. Soaking brown rice also provides more vitamins and minerals than unsoaked brown rice or white rice. And keep in mind that the fiber in brown rice, soaked or not, contributes to a healthy diet. The apple cider vinegar helps in the soaking process.

After draining and rinsing your rice, put in a large soup pot with 5 cups of water and bring to a boil.  Reduce heat and simmer for 60 minutes with the lid on. This becomes rice porridge.

Now round up all your ingredients and prepare them. I hope you enjoy this delicious and healthful soup your entire family will love. Not only will it warm you up, but will strengthen and support your healthy body.

ASPARAGUS BASIL & RICE SOUP

Printable Recipe

Serves 8

Rice Porridge

5 cups water

1 cup soaked brown rice (soak overnight in 3 cups water & 1 tablespoon apple cider vinegar)

Bring 5 cups of water to a boil with the brown rice that has been soaked overnight. Reduce temperature and simmer for 60 minutes with lid on. After 60 minutes you will have a rice porridge.

 

Vegetables  

1 lb. asparagus chopped into 1 inch pieces

1 (15 oz.) can cut baby corn drained (cut into smaller pieces as desired)

5-10 oz. cherry tomatoes cut in half

Vegetable broth 

4 cups vegetable broth

4 cups water

3 teaspoons sea salt 

Pesto 

3/4 cup chopped fresh basil

1 tablespoon nutritional yeast

1/4 cup raw pumpkin seeds

1/2 cup olive oil

Place in mini food processor and process until smooth scraping sides as needed.

Creating the soup 

To the rice porridge add vegetable broth, water, sea salt and asparagus.  Bring to a boil and then simmer for about 10 minutes, or until the asparagus is tender. Add baby corn, cherry tomatoes and pesto.  Season as needed.  ENJOY!!

 

Victor Fuchs on health reform

I've never met Victor Fuchs, but I've admired and learned from his writings for years. His article in this week's JAMA on "How and Why US Health Care Differs From That in Other OECD Countries" is a gem. Here's a summary:

US expenditures differ from the average OECD country in three ways:

1. As a percentage of GDP, US expenditures are twice as high.
2. The share of expenditures funded by government in the US is 46%, compared to a 75% average for other OECD countries.
3. The mix of services differs substantially - intense focus on technology vs more basic care.

Here's how Fuchs explains the difference, again in a series of three:

1. The US population has a much more distrustful attitude towards government - a trend with deep historical roots.
2. The US population is much less committed to equal outcomes through redistributive policies.
3. The US political system provides many "choke points" that allow special interests to block or reshape reform efforts.

Finally, Fuchs draws three practical conclusions for future reform efforts:

1.  "[G]overnment's role should be limited to what is necessary, not just desirable."
2. "[P]rovision of basic coverage for all should not require equality for obtaining additional coverage...individuals should be free to purchase more than basic care."
3. "[R]eform should have features that would appeal to some special interests, or to some elements within each special interest group."

Fuchs, who is presumably in his mid 80s (he graduated from NYU in 1947), is giving us the gift of his wisdom. His two page JAMA piece ends this way:

Comprehensive health care reform in the United States is necessary to avoid a financial disaster, but enactment of such reform will require attention to US history, values, and politics."

Fuchs' analysis is relevant for liberal critics of the Affordable Care Act. In the eyes of single payer advocates and other progressives, the ACA is a disappointing flop. But by Fuchs' three practical conclusions, the ACA was the best that could be achieved in 2010. The right approach for progressives is to do all we can to make it work.