Low GI – The Ideal Weight Loss Diet? Ben Loughrey, Medical Student
Obesity and diabetes are now considered as two of the main issues in public health. Diet has long been associated with health and as a result, many diets have been devised in attempt to improve the health of the general population. There are a number of factors to consider when evaluating diet, two of which are the glycaemic index (GI) of the diet and the glycaemic load (GL) of the diet. There is some controversy surrounding these factors and there is yet to be a definitive answer as to whether a diet based on low GI and GL foods will have any health benefits or assist in weight loss. Low GI diets have been proposed to have benefits towards cardiovascular risk factors, development of diabetes and obesity (1). Several studies have demonstrated benefits of a low GI diet over the conventional low fat high carbohydrate diet and adherence to a low GI diet and exercise appears to be a reasonable alternative in the future of weight management.
Obesity is a major public health issue in many Western countries and could soon come to have impacts further afield as social attitudes to food and consumerism change worldwide. Along with the direct effects of obesity such as hyperinsulinaemia, insulin resistance and hypertriglyceridaemia, there are also secondary public health issues to consider, such as cancer, cardiovascular incidents and mental health problems. The search is continuing for the optimum diet to reduce or control all of these risk factors. One of the diets thought to do this is a low GI or low GL diet.
Now that obesity rates are continuing to rise, physicians are now seeking out more efficient methods of weight loss and the concept of a low GI diet has come to the fore. The GI was first introduced in 1981 by Jenkins et al. as an attempt to manage the health of diabetic patients (2,3). Large meta-analyses are beginning to be presented and low GI diets have been tested in the management of obesity (1,5-10) and have shown some promise. Prescription of a low GI diet may be a better option than current dietary guidelines in decreasing obesity and obesity related morbidities. This paper examines the evidence for and against the prescription of a low GI or low GL diet for weight loss.
Definition of Low Glycaemic Index and Low Glycaemic Load
The GI represents a measure of the glycaemic response to ingestion of a fixed amount of carbohydrate in a food under question to a reference food, which is normally white bread or glucose (3,6,11). It is important to note that glycaemic index is specific to an individual (3), which is something that is impractical to take into account when performing studies on larger populations. Another way to describe GI is “the incremental area under the glucose response curve after the intake of 50g of carbohydrate from a test food compared with the area under the glucose curve induced by the same amount of carbohydrates from ingested glucose” (2,12). The values of GI therefore range from 0-100 with glucose or white bread being equivalent to 100 and a food or drink such as water equivalent to 0.
GL is slightly different and can be defined as the product of GI and the amount of available carbohydrate (10). Some studies have quoted GL as being a more valuable measure of glycaemic response (3).
Although GI and GL have been clearly defined there is yet to be a definitive statement on when a GI or GL value can be classified as high or low.
Factors Affecting the GI of Foods
The GI and physiological effects of a food are influenced by the contents of the food itself and its method of preparation. Most obviously, a food higher in glucose and other more easily digestible sugars will be more likely to elicit an accentuated glycaemic response.
Fat and protein also influence the GI of a food. Jenkins et al found a significant negative relationship between protein (r=-0.523, p<0.001) r="-0.386,">
Jenkins et al originally concluded that dietary fibre had no relationship with glycaemic index (2). Later studies have confirmed that GI is not influenced by fibre, but rather by alteration of the internal structure of the food (5). Pawlak et al used the example of comparing the GI of white bread to the GI of wholemeal bread, the result being 70 vs. 69 respectively (5). At least one study has increased fibre in an interventional trial in order to decrease the GI of the diet in question (12). This makes the results of such studies questionable.
Riccardi et al looked in detail at the ability of food properties to reduce alpha-amylase accessibility and therefore their impact on GI (12). Viscosity, resistant starch, sugars and dietary fibres were ruled out as influences on post-prandial glycaemia. Porosity however, was said to increase GI by allowing a greater surface area of food to be exposed to digestive enzymes (12). This may also contribute to the high GI of bread. Riccardi et al also note the importance of the method of food preparation in influencing the GI of a meal (12).
Hormonal Effects of GI
The hormone most obviously influenced by GI is insulin. Numerous studies have found that high GI meals tend to cause post-prandial hyperinsulinaemia (6,8,10). The anabolic effects of insulin include lipogenesis and increased fatty acid uptake (10). Insulin also has the anti-catabolic effect of inhibiting lipolysis (10). By decreasing GI and therefore insulin secretion, a decrease in fat mass is targeted. Prolonged exposure to a high GI diet resulting in chronic hyperinsulinaemia is thought to be a mechanism in diabetogenesis (13) and increased cardiovascular disease risk (Figure 1) (12). Through insulin, GI could also have secondary effects on the hormone leptin via action with other neuropeptides (11). It has been speculated that a high GI meal acts with these neuropeptides act to increase leptin concentrations, in turn having an anorectic effect (11).
Figure 1
Increased cardiovascular risk imposed by high GI foods. (12)
Low GI meals have been found to induce greater amounts of cholecystokinin and glucagon-like peptide 1 secretion (8,13). Cholecystokinin is a hormone which activates pancreatic enzyme production and secretion, contraction of the gall bladder and promotes a decrease in food intake, all of which benefit a negative energy balance.
Glucagon-like peptide-1 has been linked to GI in a similar way to cholecystokinin (8). Because lower GI foods spend a longer time in the duodenum they are thought to increase the feedback of glucagon-like peptide-1 to the satiety centre in the brain (14). The beneficial actions of these hormones on the satiety centre in the brain lend support to the use of a low GI diet in the ad libitum unsupervised setting that people live in.
Negative hormonal effects of a high GI diet include increases in cortisol and noradrenaline as a counter-regulatory mechanism (8) to increase blood glucose and prevent rebound hypoglycaemia.
Hypothesised Benefits of Low GI Diets
Weight Loss and GI
It is important to note that whilst many diets fulfil their targets of weight loss, many of them do so in an unhealthy way. A low GI diet has been proposed as a more healthy way to control and lose weight. The main arguments for low GI diets are that they encourage weight loss due to increased satiety (7), lower post-prandial insulin peaks (8), maintain the sensitivity of the body to insulin (8,10), preserve lean mass (15-17) and decrease central adiposity(8).
The hypothesised effect of a low GI diet on satiety is one of the factors that supports the application of low GI in a clinical setting. In everyday life patients have the option to eat as much of what they want and when they want. A low GI diet has been hypothesised to have beneficial effects when administered in an ad libitum setting. A feeling of satiety due to a lower GI may be down to two reasons; the physical presence of food in the stomach and duodenum and the effects of the food on blood glucose levels via hormonal pathways previously alluded to in this paper (13).
Riccardi et al acknowledged the benefits demonstrated thus far by short term studies of GI and satiety, but speculated over the longer term effects of a low or reduced GI diet on satiety and whether any correlation would have enough power to influence weight loss (12).
Buyken et al examined the breakfast dietary habits at ages 2, 4-5 and 7 years old of 381 children (11). At all of these ages a lower GI breakfast was associated with a shorter time to a subsequent meal (Figure 2) (11). The supposedly short term satiating effects of a high GI breakfast also persisted throughout the day and so performed better in satiety than a low GI breakfast (11). Despite these results Buyken et al list numerous factors which may have skewed their results including a small sample in the higher GI tertile (n=33), differing protein content amongst groups and an inability to adjust for physical activity (11).
Figure 2
Results of time to second meal according to tertile of GI. “Mean and 95% CI shown and adjusted for energy, energy-adjusted residuals of carbohydrate and protein, and consumption of caloric beverages (in grams) at breakfast. Group 4-5 years also adjusted for age”(11)
Ball et al had conflicting results to Buyken et al when examining variation in satiety in response to a low GI meal replacement, a low GI whole food meal and a moderately high GI meal replacement (18). Ball et al used three indices to assess satiety; hunger scales, time to snack platter requests and voluntary energy intake (18). Interestingly, the different scales produced varying results representative of satiety. The hunger scale showed no difference in satiety between meals, as did voluntary energy and macronutrient intake, but food was requested sooner after the moderately high GI meal replacement. The most significant result in time to snack request was between the low GI meal replacement and the high GI meal replacement (p ≤ 0.01) (18). Despite the significant result in time to snack request, the number of snacks requested by subjects was the same by the time the following meal was presented (18). Ball et al hypothesised that these results may be because there is no satiety difference between low and moderately high GI meals or that intake of food could be modulated by external cues more so than hunger (18).
Whilst most studies assess satiety according to subsequent meal consumption there may be social and cultural influences which influence the intake of food. Some subjects may simply eat more frequently out of habit and so consume more food regardless of the GI. Likewise, a similar situation could skew any attempt to assess satiety using visual analogue scales, such as in the study by de Rougement et al (1).
According to Pittas et al a low GI diet allowed more weight loss in overweight individuals with relatively higher insulin secretion than those who were overweight with low insulin secretion (10). Thirty two participants completed the trial and the necessary measurements over a six month period (10). Those with a high baseline insulin value thirty minutes after a 75g oral glucose tolerance test (INS-30) lost more weight when on a low GI diet (p<0.05)(10).>und in those with a low INS-30 result, although the difference was not significant (p = 0.25) (10).
Raatz et al conducted a thirty six week prospective, three arm, parallel group trial of which twenty two of a potential forty two participants completed (6). Six subjects were assigned to a low GI diet, eight to a high GI and eight to a high fat (HF) diet (6). Each diet was hypocaloric and separated into a twelve week feeding phase proceeded by a twenty four week free-living phase (6). After 12 weeks each group had lost weight (p<0.001),> greater improvement than the HF group (6). On completion of the study Raatz et al found that weight loss was independent of diet composition and so concluded that lowering the GL and GI of a diet did not have added benefit to weight loss in obese subjects (6). This conclusion is unjustified, as at twenty four weeks the GIs of the diets differed (p=0.014) and after thirty six weeks the glycaemic indices of the groups did not differ (p = 0.14) (6). Three diets of similar GI were effectively being compared against one another for the final twelve weeks of the study, thus calling into question the conclusions drawn.
A further study examining the influence of GL on weight loss provided evidence that a reduced GL diet could be used in alternative to the conventional low-fat hypocaloric diet (9). In this study, after thirty six weeks the reduced GL group had lost more weight than the control group, although not significant (p=0.684). The amount of fat mass lost was significant at the thirty six week point, with the reduced GL group losing 2.1kg±0.3kg and the control group losing 0.9kg±0.3kg (p=0.004) (9). Whether the loss of fat free mass was lean tissue or water was not stated in the literature.
In recent years health professionals have begun to move away from the use of BMI in assessing obesity status. Instead, a waist to hip ratio is becoming more commonly used, as central adiposity is a being accepted as a better indicator of health.
Brand-Miller et al state that the overall GI of a diet is an independent predictor of waist circumference in men and thus a low GI diet may act to decrease abdominal adiposity (8). In a study identified by Raben et al, there was no difference in bodyweight and ad libitum energy intake, but there was a decrease in fat mass, mainly in the abdominal area on a low GI diet (7). This finding also suggests that a low GI diet could help increase the lean mass of the body.
Raatz et al also found the results from ten subjects on a low GI diet in a 36 week trial showed a decrease in body fat with a preservation of lean mass. This result may be partially explained by trends showing that low GI foods cause preferential fat oxidation (19).
In a number of longer term studies a low GI diet has been found to not only encourage immediate weight loss, but also to outperform a low fat diet in the maintenance of weight loss (5,6,8).
GI and Diabetes
GI is closely associated with diabetes and was first introduced as a means of management of diabetic patients (2). Diets with a high GI tend to cause post-prandial hyperinsulinaemia. This in turn results in weight gain as the anabolic effects of insulin include lipogenesis and increased fatty acid uptake (10). Insulin also has the anti-catabolic effect of inhibiting lipolysis (10). By decreasing the GI or GL of a diet greater control may be exercised over post-prandial insulin and may potentially protect against the development of type II diabetes (Figure 3) (12).
Figure 3
Diagrammatic representation of hypothesised influence of high GL on type II diabetes. (12)
A study on sixty three type I diabetes patients assigned to a low GI, high fibre diet or a high GI, low fibre diet found that the low GI high fibre diet decreased mean daily blood glucose concentrations (p<0.05)>nce of hypoglycaemia (p<0.01)>
De Rougement et al found no significant increase in insulin sensitivity after prescription of a low GI diet in overweight non-diabetic subjects (1); however Pittas et al found that a low GL diet was of more benefit to hyperinsulinaemic patients (10). Slabber et al also found similar results in a trial of thirty two obese hyperinsulinaemic women (20). However, certain conclusions can be drawn on these potential positive effects of low GL diets as further trials are required using larger numbers of patients (10).
GI and Serum Lipids
Hyperlipidaemia is another major public health issue and is a complication related to the conventional low fat diet. A number of studies have found beneficial effects of a low GI on serum cholesterol and serum triglycerides (3,9). This potential benefit of a low GI diet may indicate that it should be utilised in preference to a low fat diet.
Insulin has the effect of stimulating VLDL cholesterol synthesis, therefore a low GI or low GL that decreases insulin secretion would be expected to have positive effects on serum VLDL cholesterol and thus cardiovascular risk factors (9).
Mosdol et al found an inverse relationship of both GI and GL with HDL cholesterol and a direct relationship with GI and serum triglycerides (3). This prospective study was carried out on 7321 participants over a period of 13 years (3). After adjusting for alcohol intake, smoking status, physical activity and employment grade the relationship of GI and GL with HDL cholesterol remained, although after adjusting for fibre and carbohydrate intakes the significance of the results was markedly decreased (3).
Ludwig et al examined potential relationships between dietary GI and obesity, diabetes and cardiovascular disease in a meta-analysis of 13 interventional studies (13). The majority of these studies demonstrated a low GI diet to have beneficial effects on serum triglycerides, low density lipoprotein (LDL) cholesterol and high density lipoprotein (HDL) cholesterol (Figure 4) (13). Ludwig et al also found increased serum free fatty acid concentrations after consumption of a high GI meal and hypothesised that this may impair the function of pancreatic beta cells by the process of lipotoxicity (13)
.
Figure 4
Percentage change in lipid concentration in comparison of a low GI diet with a high GI diet (13).
Harbis et al investigated the effect of hyperinsulinism on apolipoprotein B-48 and found a positive relationship between an acute insulin response and post-prandial apolipoprotein B-48 levels (20). If these results were applied to dietary advice then a low GI diet would be favoured in order to avoid elevated insulin and resultant apolipoprotein B-48 increase.
In a randomised control trial undertaken by Maki et al forty three subjects were prescribed an ad libitum reduced GL diet and forty three a low-fat portion-controlled diet (9). Subjects who were following the reduced GL diet had higher total, saturated and unsaturated fat intakes than the participants who followed the low fat portion controlled diet. The differences in the fat intakes of the groups, however, were not significant. Mean dietary cholesterol was also higher in the reduced GL group than in the other arm of the study (p<0.001). p="0.037)">
De Rougemont et al discovered slightly different variations in serum cholesterol following a five-week interventional trial on thirty eight overweight non-diabetic subjects (1). Nineteen subjects were assigned to a low GI (<50)>70) diet (1). Those following the low GI diet had a significant 8.6% decrease in LDL-cholesterol compared to a 3.7% decrease in the high GI arm of the study (1). Contrary to other study results the low GI arm of the study had a decrease of 2.5% in HDL-cholesterol (1). Considering the decrease in HDL cholesterol, the low GI was still superior in improving lipid profile because of the large decrease in LDL-cholesterol improving the lipid ratios and thus cardiovascular risk (1).
Despite a number of studies discovering positive effects of dietary GI on serum lipids, a prospective study undertaken by Abete et al found no significant changes in serum lipids when comparing a higher GI diet to a lower GI diet (22) (Table 1).
Table 1. Results of an eight week trial of dietary GI on serum lipids. Adapted from Abete et al. (22)
| Higher-GI diet (n=16) | Lower-GI diet (n=16) |
| |||
| | Baseline | Change (%) | Baseline | Change (%) | Statistical Significance between baseline points | Statistical significance between changes (%) |
| Total cholesterol (mg/dl) | 181 ± 34 | -3.5 ± 10.6 | 215 ± 37 | -14.4 ±10.5 | 0.014 | 1.010 |
| LDL-c (mg/dl) | 112 ± 29 | -3.2 ± 14.3 | 136 ± 5 | -15.9 ± 16.6 | 0.124 | 0.037 |
| HDL-c (mg/dl | 51 ± 9 | -5.5 ±14.9 | 50 ± 12 | -9.7 ± 8.1 | 0.935 | 0.348 |
| Triglycerides (mg/dl) | 89 ± 28 | 5.1 ± 40.8 | 97 ± 36 | -2.4 ± 18.0 | 0.513 | 0.531 |
Effects of GI on Mitochondrial Oxidation
Abete et al. examined the association between GI and mitochondrial oxidation using the 2-keto[1-13C]isocaproate breath test (22). 2-keto[1-13C]isocaproate is a keto acid metabolised exclusively by mitochondria. By measuring the decarboxylation of this compound the rate of mitochondrial oxidation can be estimated (22). The results were significant for both the subjects prescribed the low GI diet and those prescribed the high GI diet (22). In those who had undertaken the low GI diet 2-keto[1-13C]isocaproate oxidation was significantly increased (p=0.022) and in those who had undertaken the high GI diet 2-keto[1-13C]isocaproate oxidation was also significantly decreased (p=0.022) (22).
After further separate regression analyses Abete et al (22) found that the lower GI diet increased mitochondrial oxidation by 3.5-fold in comparison to the higher GI diet (corrected r2 = 0.61; p<0.001).>
Figure 5
Percentage changes in mitochondrial oxidation are displayed to the right. The asterisks demonstrate that mitochondrial oxidation was significantly altered after nutritional intervention (22).
Despite the promising results of this study on mitochondrial oxidation, the study was small, with only thirty-two obese subjects participating in the trial and a study power on the lower border of conventionally acceptable (80%) was targeted. Abete et al. also used legumes to reduce the GI of the subjects’ diets rather than altering the actual carbohydrate constituents themselves (22). Therefore, it is possible that the changes observed may not be due to the difference in GI, but due to constituents of the legumes, for example minerals or antioxidants.
Conclusion
From a thorough analysis of available literature there appears to be a lot of evidence supporting administration of low GI foods to support weight loss, particularly in overweight and obese subjects. Studies have found that a low GI diet can positively influence HDL and LDL cholesterol levels, improve mitochondrial oxidation and aid long term weight loss.
Although studies display many positive aspects to a low GI diet, most of the trials conducted on patients did not use any indicators of quality of life, one of the most important aspects to take into consideration when amending lifestyle factors in patient care. There are many conflicting results in studies examining the affects of a low GI diet in weight loss, but in all studies a low GI diet did produce weight loss and in the majority it performed as well, or better than a low fat diet. In studies on low GI and serum lipids a low GI had benefits in improving lipid profile, something which supports its use in preference to a low fat diet. After considering the study on mitochondrial oxidation and low GI by Abete et al (22) it would be premature to conclude that a low GI diet has benefits in mitochondrial oxidation.
In conclusion, from the results available, a low GI diet is a good alternative to the conventional low fat, high carbohydrate diet and results suggest good patient compliance. It appears to display all the positive weight loss benefits of a low fat, high carbohydrate diet, without adverse affects on indicators of cardiovascular wellbeing (11). It cannot yet be considered the ideal weight loss diet, but prescription of a low GI diet along with exercise should be investigated further by health authorities as a modern alternative to the currently recommended low fat diet, high carbohydrate diet.
References
(1) de Rougemont A, Normand S, Nazare JA, Skilton MR, Sothier M, Vinoy S, et al. Beneficial effects of a 5-week low-glycaemic index regimen on weight control and cardiovascular risk factors in overweight non-diabetic subjects. Br.J.Nutr. 2007 Dec;98(6):1288-1298.
(2) Jenkins DJ, Wolever TM, Taylor RH, Barker H, Fielden H, Baldwin JM, et al. Glycemic index of foods: a physiological basis for carbohydrate exchange. Am.J.Clin.Nutr. 1981 Mar;34(3):362-366.
(3) Mosdol A, Witte DR, Frost G, Marmot MG, Brunner EJ. Dietary glycemic index and glycemic load are associated with high-density-lipoprotein cholesterol at baseline but not with increased risk of diabetes in the Whitehall II study. Am.J.Clin.Nutr. 2007 Oct;86(4):988-994.
(4) Thomas DE, Elliott EJ, Baur L. Low glycaemic index or low glycaemic load diets for overweight and obesity. Cochrane Database of Systematic Reviews 2007(3):005105.
(5) Pawlak DB, Ebbeling CB, Ludwig DS. Should obese patients be counselled to follow a low-glycaemic index diet? Yes.[see comment]. Obesity Reviews 2002 Nov;3(4):235-243.
(6) Raatz SK, Torkelson CJ, Redmon JB, Reck KP, Kwong CA, Swanson JE, et al. Reduced glycemic index and glycemic load diets do not increase the effects of energy restriction on weight loss and insulin sensitivity in obese men and women. J.Nutr. 2005 Oct;135(10):2387-2391.
(7) Raben A. Should obese patients be counselled to follow a low-glycaemic index diet? No.[see comment]. Obesity Reviews 2002 Nov;3(4):245-256.
(8) Brand-Miller JC, Holt SH, Pawlak DB, McMillan J. Glycemic index and obesity. Am.J.Clin.Nutr. 2002 Jul;76(1):281S-5S.
(9) Maki KC, Rains TM, Kaden VN, Raneri KR, Davidson MH. Effects of a reduced-glycemic-load diet on body weight, body composition, and cardiovascular disease risk markers in overweight and obese adults. Am.J.Clin.Nutr. 2007 Mar;85(3):724-734.
(10) Pittas AG, Das SK, Hajduk CL, Golden J, Saltzman E, Stark PC, et al. A low-glycemic load diet facilitates greater weight loss in overweight adults with high insulin secretion but not in overweight adults with low insulin secretion in the CALERIE Trial. Diabetes Care 2005 Dec;28(12):2939-2941.
(11) Buyken AE, Trauner K, Gunther AL, Kroke A, Remer T. Breakfast glycemic index affects subsequent daily energy intake in free-living healthy children. Am.J.Clin.Nutr. 2007 Oct;86(4):980-987.
(12) Riccardi G, Rivellese AA, Giacco R. Role of glycemic index and glycemic load in the healthy state, in prediabetes, and in diabetes. Am.J.Clin.Nutr. 2008 Jan;87(1):269S-274S.
(13) Ludwig DS. The glycemic index: physiological mechanisms relating to obesity, diabetes, and cardiovascular disease.[see comment]. JAMA 2002 May 8;287(18):2414-2423.
(14) Lavin JH,
(15) Bouche C, Rizkalla SW, Luo J, Vidal H, Veronese A, Pacher N, et al. Five-week, low-glycemic index diet decreases total fat mass and improves plasma lipid profile in moderately overweight nondiabetic men. Diabetes Care 2002 May;25(5):822-828.
(16) Stevenson E, Williams C, Nute M. The influence of the glycaemic index of breakfast and lunch on substrate utilisation during the postprandial periods and subsequent exercise. Br.J.Nutr. 2005 Jun;93(6):885-893.
(17) Wee SL, Williams C, Tsintzas K, Boobis L. Ingestion of a high-glycemic index meal increases muscle glycogen storage at rest but augments its utilization during subsequent exercise. J.Appl.Physiol. 2005 Aug;99(2):707-714.
(18) Ball SD, Keller KR, Moyer-Mileur LJ, Ding YW, Donaldson D, Jackson WD. Prolongation of satiety after low versus moderately high glycemic index meals in obese adolescents. Pediatrics 2003 Mar;111(3):488-494.
(19) Wolever TM, Gibbs AL, Mehling C, Chiasson JL, Connelly PW, Josse RG, et al. The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y controlled trial of low-glycemic-index dietary carbohydrate in type 2 diabetes: no effect on glycated hemoglobin but reduction in C-reactive protein. Am.J.Clin.Nutr. 2008 Jan;87(1):114-125.
(20) Slabber M, Barnard HC, Kuyl JM, Dannhauser A, Schall R. Effects of a low-insulin-response, energy-restricted diet on weight loss and plasma insulin concentrations in hyperinsulinemic obese females. Am.J.Clin.Nutr. 1994 Jul;60(1):48-53.
(21) Harbis A, Defoort C, Narbonne H, Juhel C, Senft M, Latge C, et al. Acute hyperinsulinism modulates plasma apolipoprotein B-48 triglyceride-rich lipoproteins in healthy subjects during the postprandial period. Diabetes 2001 Feb;50(2):462-469.
(22) Abete I, Parra D, Martinez JA. Energy-restricted diets based on a distinct food selection affecting the glycemic index induce different weight loss and oxidative response. Clinical Nutrition 2008 Aug;27(4):545-551.
2 comments:
It was painstaking trying to get this up in some sort of legible format. Sorry that the images are really small
Interesting read, even if I didn't get the second half much.
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